Pneumonia. Etiology

Pneumonia - about. infection Mostly bacterial etiology, the Har-smky lesion of the respiratory departments of the lungs, the presence of inhabitricular exudation, detected in physical and / or intoximal research, expressing. In varying degrees of feverish reactions and intoxication.

Etiology: Strept.pneum., Haem.infl., Mycopl.pneum., Chlamid. Pneum., Moraxella Cataralis, Klebs. Pneum., Legionella Pneum.; Staph.aureus, Pseud.aeruginosa, Klebs.spp, Enterobacter SPP, E.Coli - Gospet.

Pathogenesis: mechanisms Obuslaving the development of Mon. - aspiration of the rotoglot; Inhalation of aerosol containing in-la; Hematogenic propagation from an extralegal focus of infection (endocarditis, thrombophlebitis); Directly propagation of infection from adjacent affected tissues (liver abscess), infection with penetrating injuries of the GC.

CLASSIFICATION:

· Complete-hearth

1. Persons under 60

2.\u003e 60 years Against the background of concomitant pathology (XP. Bronchildren's Bronchildren System, IBS, SD, etc.)

· Intro-community (hospital, nosocomial) - purchased inside LPU

· Aspiration

· Pneumonia in persons with IDC (congenital or acquired)

· By etiology: ...

· In clinical and morphological features: parenchymal, interstitial

· Localization: right-sided, left-sided, bilateral, segmental, share, brunt,

· According to severity: lightweight, medium, heavy

CLINIC: Complaints:weakness, loss of appetite, shortness of breath, chest pain, cough - dry -\u003e sputum (from mucous to purulent, + streams of blood). Physician: Pallor, cyanosis. Sharp t 0 (bruboral pneumonia). Strengthening voice tremors on the side of the lesion + bronchial respiration (drain + brunt pneumonia). Shortening of the percussion sound above the lesion center (with a lesion of more than 1 segment). At bronchopneumonia - dry and wet wives. The noise of friction is pleura (dry pleurisy). A sharp weakening of breathing - in the formation of pleural effusion. Bronchophony. Accent II tone over the pulmonary A. for severe flow. R-OGK: foci of inflammatory infiltration in the form of fuzzy dimming.

Complete pneumonia:

1) Typical pneumonia syndrome: sudden fragile fever, cough with purulent sputum, pleurritic chest pain, signs of lung tissue (rebuilding of percussion sound, vocal trembling, bronchial breathing, wheezing in R-change projections). Etiology: Strept.pneum., Haem.infl. + Mixed oral flora.

2) Atypical pneumonia syndrome: gradual start, dry cough, predominance outside pulmonary symptoms (headache, pain in mm, weakness, angina, nausea, vomiting, diarrhea) + r-picture with minimal signs of physical examination. Etiology: mycopl.pneum., Chlamid. Pneum., Moraxella Cataralis, Klebs. Pneum., Legionella Pneum. Main manifestations: fever, tachipne, mental disorders.

Nosocomial pneumonia: Dn is competent with the appearance of pulmonary infiltrate after 48 h and\u003e after hospitalization. Typical criteria: purulent wet, fever, L-cytosis.

Aspiration pneumonia: Rifle sputum, necrosis of the pulmonary tanya with the formation of a cavity in the lungs (abscess), cough, pleurritic pain.

COMPLICATIONS: 1. pulmonary (empiama pleura, exudate. pleurisy, abscess and gangrena lung, broncho-constructive syndrome, One) 2. Outlogochny (o. Pulmonary heart, ITS, meningitis, meningoencephalitis, nonspecific endo-, mio-, pericarditis, DVS, glomerulonephritis, anemia).

TREATMENT. Indications for hospitalization: Age\u003e 70 years, accompanying xp. Diseases (COPD, stagnant CH, XP. Hepatitis, XP. nephritis, SD, IDC, alcoholism, toxicomination), inefficient outpatient treatment for 3 days, confusion or depression of consciousness, possible aspiration, ChDD\u003e 30 per minute, unstable hemodynamics, Septic shock, infectious MTS, exudative pleurisy, abscess, L-singing< 4х10 9 /л или L-цитоз > 20x10 9 / l, HB< 90 г/л, почечная недостаточность (мочевина > 7 mmol / l).

· Antibiotic therapy

Complete Pneumonia:

1) Patients< 60 лет без сопутствующей патологии

Amoxicillin, macrolides.

Alternative: doxycycline, fluoroquinolones with antiphenmococcus. Activity (Levofloxacin, Moxifloxacin)

2)\u003e 60 years and / or with the housing pathology:

Amoxicillin incl. with clavulone + Macrolids or Cephalosporins II II + macrolides;

Alternative: Fluoroquinolones with antiphenmococcus. Activity

3) clinically heavy pneumonia regardless of age

Partner. Cephalosporins III of generation (cefatoksim, ceftriaxone) + partner. macrolides;

Alternative: Partner. Fluorokinolone.

Hospital pneumonia:

1) Depositary .Prof. Without risk f-me, Pete - "Early" WAP

Partner. Cephalosporins III of generation,

Alternative: fluoroquinolones, antsingenic cephalosporins III-IV Pain. (Cephipim, ceftazidine) + aminoglycosides.

2) "Late" WAP, deposit. + Risk

Carbopenmes (Tienam)

Cephalosporins III-IV Pok. + Aminoglycosides

Antsynegn.penicillins (peperacyllin) + aminoglycosides

Azzleon + Aminoglycosides

Fluoroquinolones

Glycopeptides (Vancomycin)

Aspiration pneumonia: Anti-Anaerobic Preparations

Protected Betalaktama, Cefoatoxim, Cefmethason

Carbopenmes (TIENAS, IMIPENEM)

· Pathogenetic and symptomatic therapy

1. Immunoocitor therapy: SPP, Normal Ig Human 6-10g once.

2. Correction of microcirculation: heparin.

3. Dispretinemia correction: albumin, nandrolol.

4. Disinfection

5. O 2 -Cingpius

6. GKS: Prednisolone.

7. Antioxidant therapy: ascorbic acid 2g / day inside.

8. Antimement drugs: apricin

9. Broncholitics (in the presence of instrumentally verified obstruction): Bromide, Salbutamol.

10. Expectorant preparations inside: ambroxol, acetylcysteine.

· Non-media treatment

Sparing mode, full nutrition, abundant drink. LFK. Sanatorium-resort treatment: lowland, forest zones, warm, moderately wet marine climate.

Acute pulmonary suppuration- Abscess, gangrenoz abscess and gangrene of the lungs are severe pathological conditions characterized by sufficiently massive necrosis and subsequent purulent or rotten decay (destruction) of pulmonary tissue as a result of infectious pathogens.

The main causative agent for sharp pulmonary suppurationcondected aspiration of orofaring towing mucus are non-cryological (unfortunate) anaeros. They usually exist in large quantities and saprofit in the oral cavity in periodontal disease, the caries of the teeth, the pulpit and others.

The main causative agent for para- and metapneumonic, hematogenic-embolistic pulmonary suppurationsare gram-negative aerobes and conditionally anaerobic bacteria, as well as global cocci. With hematogenic-embolocal pulmonary destruction, golden staphylococcus is most frequent causative agent.

The respiratory viral infection is often active on the course and outcome of sharp pulmonary suppuration.

According to the alleged pathogenesis, sharp pulmonary suppurations are divided into: i) bronchogenincluding aspiration, postpnemonic, obtuctive;2) hematogenic;3) traumatic;4) otherfor example, associated with a direct transition of suppuration from neighboring organs and tissues.

Most frequent complicationspulmonary suppurations are tupupnemothorax, empieme pleural, pulmonary bleeding, bacteremic shock, acute respiratory distress - syndrome adults septis, phlegmon chestand etc.

Gangrena lung - Progressing necrosis and ypokhorozny (rotten) disintegration of lung fabric, not inclined to limit.

The disease is inherited by recessive type, as a rule, is not transmitted from parents to children.

Etiology.The causative agents of the disease are non-crystridial anaerobes.

Diseases as chronic alcoholism, diabetes, pneumonia in weakened patients predict to the development of lung ganglenes. Direct reasons can be: penetration into the respiratory tract foreign languages, bruboral inflammation of the lungs, dust or echinococcus in light; Various diseases of blood vessels.

The immunological and non-immunological forms of the lung gangrene are distinguished, there are also a number of options: atopic, infectious-allergic, dormriconal, autoimmune, neuropsychic, adrenergic imbalance, primary changed reactivity of bronchi, cholinergic.

Pathogenesis.Anaerobic bacteria penetrate the pulmonary tissue, the bacterial exotoxins are activated and their immediate effects on the pulmonary tissue, progressive necrosis of the pulmonary tissue, vessel thrombosis in the damage zone, impairment of granulation tissue.

Clinic.The main manifestations of the disease are cough with stencil sputter and fragments of the pulmonary tissue, the hectic nature of fever, the pain in the chest, shortness of breath, perfectly at the beginning of the disease, the expanding stupidity is determined; During the period of the rank - the appearance of plots of tympanite due to the formation of cavities. During palpation, soreness is determined above the zone of the lesion (symptom of kitesling) and percussion (Sauerbroha syndrome) (involvement in the process of the pleura), palpatorially - at first an increase in voice trembling, then weakening. Auscultation is heard at the beginning of bronchial breathing, then a sharp impact of breathing.

Additional diagnostic study.Held general analysis Blood, where neutrophilic leukocytosis is determined with a sharp shift to the left, enlarged ESO. The wet survey is also carried out (with a sputum macro-examination forms 3 layers: the upper - frothy, liquid; medium - serous; lower - scraps of disintegrating lung tissue; microde study - study of flora, cytology), x-ray study (massive infiltration without clear boundaries with the presence of multiple merging cavities irregular shape).

Differential diagnosis.Must be carried out with tuberculosis, lung cancer.

Flow.The course of the disease is severe, progressive.

Treatment.Antibacterial therapy (parenterally, intravenous) is carried out, it is possible to introduce into the pulmonary artery. Combine several types of antibacterial drugs. Disinfecting therapy (REOOPOLIGLUKIN, hemodez, hemo-sorption, UVO autobroviya), bronchospasmolytic therapy, endoscopic reservation of bronchi, followed by the introduction of antibiotics, enzymes, antiseptics, hemotransphus (with the development of anemia), are applied by heparin (for the prevention of DVS syndrome),

Prevention.Prevention measures include adequate treatment of sharp pneumonia, adequate bronchial drainage, shanction of chronic infection, refusal of smoking.

Abscess light- Limited purulent inflammation of pulmonary fabric with destruction of its parenchyma and bronchi, their melting and the formation of the cavity.

Etiology.The obstruction of bronchi by foreign bodies, acute pneumonia, bronchiectases, chest injuries, hematogenic embolization infection.

Pathogenesis.An infectious agent penetration into pulmonary tissue (bronchogenic, hematogenous, lymphogenic path, aspiration of foreign bodies), violation drainage function Bronchi.

ClassificationAccording to the characteristics of the clinical flow, the disease is divided:

1) by origin: acute lung abscess and chronic lung abscess;

2) on localization (segment, segments, right, or left-sided);

3) by complications.

Clinic.With the acute abscess of the lung (OAL) allocate period of organization(before opening the cavity - up to 7 days), which is characterized by acute principle (dry adsatory cough, chills), changing the chill to the pouring sweat (hectic fever), mental disorders, puffiness of the face, hyperemia of the cheek, lag behind the affected side of the chest when breathing, local Cleaning a percussion sound, hard breath with a bronchial tint, and period after opening the cavitycharacterized by a sudden disorder of purulent sall sputum with a complete mouth, a drop in temperature, a decrease in intoxication. Percusser over the affected section of the lung is determined by the appearance of tympanite, with auscultation breathing amphoric, wet medium and large-tape rescurable wheels.

Introduction

Pneumonia is an acute infectious disease of the lungs, with the obligatory lesion of the alveoli and other structural elements of the lung fabric.

Pneumonia is one of the most common society diseases. According to WHO, there were 1408 patients with pneumonia (53 died). In the sickness, the disease has already been registered in the 22 countries of the world. Currently, the number of ill, reaches almost 10 thousand, and the number of dead exceeds 700. For example, in Russia annually registered among people over 18 years of about 3.9%. So, in 2009, incidental pneumonia was registered with diagnosis with a diagnosis of 117 people, in 2010 - 89 people, in 2011 - 150 people. At the same time, the etiology of most pneumonium remains unidentified. Another problem with which is constantly faced by practical doctors and researchers is the lack of an unambiguous classification of this disease. Indeed, pneumonia can act in the form of a "independent disease" and as a complication of lower infections respiratory tract (chronic obstructive bronchitis, bronchiectase), with stagnant heart failure or against the background of various forms of immunodeficiency. The relevance of the circle of problems associated with the diagnosis and treatment of pneumonia will be particularly understood if it seems to consider pneumonia as an independent disease. In this approach, for example, it turns out that in industrialized countries, pneumonia ranks 6th among all causes of mortality and 1 among infectious diseases.

Pneumonia is characterized by the development of serious complications. Among the complications that may occur with pneumonia distinguishes pulmonary and extrapulations - they largely depend on the course, outcome and possible forecast Diseases. The most frequent pulmonary complications are obstructive syndrome, acute respiratory failure, abscess and lung gangrena, exudative pleurisy.

Extractive complications of pneumonia are acute cardiovary and pulmonary failure, myocarditis, endocarditis, meningoencephalitis and meningitis, sepsis and infectious-toxic shocks, psychosis. Thus, pneumonia is a serious test not only for patients, but also for medical personnel, a successful way out of which is determined by the timeliness of the diagnosis of the onset of the disease, adequate treatment and attentive care and care for the patient. Therefore, the correct, professional and timely organized nursing process is necessary to prevent complications and largely determines the prospective forecast.

The goal of the course robots: study of the peculiarities of nursing assistance in pneumonia.

Currency tasks:

1. Conduct a comparative analysis of sources and literature relating to this issue.

2. To hold a nursing examination of the patient with pneumonia.

3. Implement the nursing process at pneumonia.

4. To issue a nursing history of the disease.

THEORETICAL PART

Etiology, pathogenesis of pneumonia.

Pneumonia is primarily a bacterial disease. The main pathogens of pneumonia are: Pneumoniae (Streptococcus Pneumoniae), Staphylococcus (Staphylococcus aureus), hemophilic stick (Haemophilus Influenzae) as well as "atypical" infections. A starting factor in the development of pneumonia can be various viral infections. They cause inflammation of the upper respiratory tract and provide good conditions For the development of bacterial pathogens. Also, pneumonia can develop due to the impact of noncommunicable factors: injuries of the chest, ionizing radiation, toxic substances, allergic agents. The risk group for the development of pneumonia includes patients with stagnant heart failure, chronic bronchitis, chronic nasopharyngeal infection, congenital lung defects, with severe immunodeficiency states, weakened and exhausted patients, patients, long-term beddown, as well as senior and senile facial .

Particularly subject to the development of pneumonia smokers and alcohol abusers. Nicotine and alcohol pairs damage the mucous membrane of the bronchi and oppress the protective factors of the bronchopulmonary system, creating a favorable environment for the introduction and reproduction of infection.

Infectious pathogens of pneumonia penetrate into light bronchogenic, hematogenic or lymphogenic paths. With the reduction of the protective bronchopulmonal barrier in Alveoli, infectious inflammation develops, which through permeable intervalolar partitions is distributed to other departments of lung tissue. In Alveola, the formation of an exudate that prevents oxygen gas exchange between the pulmonary fabric and blood vessels. Oxygen and respiratory failure develop, and with a complicated flow of pneumonia - heart failure.

In the development of pneumonia 4 stages are allocated:

The stage of the tide (from 12 hours to 3 days) is characterized by a sharp blood flow of vessels of lungs and fibrinous exudation in the alveoli;

Stage of red oven (from 1 to 3 days) - a piece of lung tissue occurs, according to the structure resembling a liver. Erythrocytes in large quantities are found in alveolar exudate;

The stage of gray compelling - (from 2 to 6 days) - is characterized by the decay of the red blood cells and the massive leakocyte output in the alveoli;

The resolution stage is restored by the normal structure of the lung tissue.

1.2 Pneumonia classification

Pneumonia distinguish:

1. According to etiology: streptococcal, pneumococcal, staphylococcus.

2. Depending on the occurrence conditions:

Extractal,

Hospital (48-72 hours)

Aspiration

In people with a heavy defect of immunity

3. Localization:

One-sided

Double-sided

4. By clinic - morphological features:

Bomber

Focal

Brewing pneumonia is pneumonia characterized by the defeat of the lungs. The causative agent can be pneumococcus, as well as other microorganisms (streptococcus) penetrating into the lungs through the respiratory tract. For the development of the disease, predisposing conditions are needed, which reduce the protective forces of the body: sharp cooling, mental overvoltage, dysfunction. Penetrating into one of the sections of the pulmonary fabric, the pneumococcus distinguishes toxin, which extends to the whole share of the lung. The permeability of the vessels increases and exudes the fibrin and blood cells in the Alveola. With bitter pneumonia, the pathological process passes several stages. In the I stage, the stage of hyperemia and tide - inflammation in Alveoloch leads to their expansion and the appearance of exudate in them. In stage II in Alveolar exudate from extended vessels, erythrocytes come. The air from the alveolo is supplanted. The alveoli filled with fibrin attached to a light liver color. This stage is called a red oven. In stage III, leukocytes prevail in the exudate. This stage is called a gray redhead. Last stage - Permit Stage: Fibrin and Leukocytes in Alveoli are absorbed and partially expectorated with a spree. The stage of the stage lasts 2-3 days, II and III (they cannot be clearly divided, since the processes of red and gray compelling are almost parallel) - 3-5 days. Permission comes to the 7th and 11th day of the disease.

Symptoms of bruboral pneumonia.

The disease, most often, begins rather sharply: there are general ailments, chills, sharp weakness, sweating, headache, on the skin of the face (nasolabial folds) - a simple herpes. Consciousness can be somewhat confused. The body temperature comes to high digits and keeps several days, and then dramatically decreases for several hours (crisis).

After the crisis, the patient's condition is improving, it begins to recover quickly. For favorable conditions The crisis comes to the 7-8th day of the disease. In this period, there may be sharp heart weakness (reduction in blood pressure, the increase and weakening of the pulse, etc.), which is important to consider the careful personnel. Cordiamin, camphor, Meston, caffeine, adrenaline for lifting blood pressure, as well as oxygen should be taken. Currently, the classic crisis pattern is rare. The use of antibiotics in the initial stages of the disease leads to the fact that the body temperature of the patient of brunt pneumonia is reduced after 2-3 days and not too sharp (lysis). One of the important early symptoms of brup pneumonia is a cough with a sputter, in which blood streaks are visible ("rusty wets"), as well as pain when breathing in the chest at the stroke of inflammation (this is due to the fact that , Plevura plots are affected, adjacent to the inflamed share of the lung). Breathing is expensive, and when inhaling the affected side of the chest is somewhat lagged. Percussion changes are particularly characteristic in the stage of gray and red comrade - above the inflamed lobes shares are determined by stupid chub. In auscultation, bronchial respiration and attitudes are listened, and then with a sputum selection in the final stage of the disease - solid-caliber wet wets. In case of truck pneumonia there are pronounced Pato logical changes in other organs and systems. We talked about some changes to the pleura. Change of cardio-vascular system Expressed in the increase in the pulse, decrease in blood pressure. If a nonstato and almost healthy person sick pneumonia, changes in the cardiovascular system, as a rule, are not much danger, then the state of the cardiovascular system has a weakened patient or an old person, it is necessary to pay the most serious attention. Some changes in the kidney function are observed, a small amount of protein in the urine. When studying blood, leukocytosis is noted - an increase in the number of leukocytes and an increase in ESR. Characteristic changes are with x-ray and radiography.

Focal pneumonia - for this pneumonia is characterized by the defeat of the lungs. The pathological process in focal pneumonia as a whole undergoes the same stages as with duty pneumonia: serous effusion in the alveoli, the step of compensation, permission. However, with focal pneumonia for a clear cyclicity and, in general, the inflammatory process is less active. The exception is the so-called metastatic purulent foci in the lungs as a result of the driving of the causative agent of infection from any peripheral purulent focus (peritonitis, liver abscess, osteomyelitis, etc.). The clinical picture of focal pneumonia is less pronounced than with a brunt. Being often secondary, focal pneumonia is absorbed by the main disease (flu, aggravation of chronic bronchitis).

Symptoms of focal pneumonia.

The body temperature increases, pain in the chest occurs due to irritation of the pleura, the cough is enhanced. These symptoms make it possible to conclude a starting focal pneumonia. In addition, during the examination, a number of objective symptoms are detected: attitudes on a limited area of \u200b\u200binflammation, bronchial respiratory sections. Radiologically noted areas of darkening of lung tissue. In the study of blood, pathological changes (leukocytosis, an increase in ESP) are less pronounced than with brunt pneumonia. General symptoms (malaise, weakness) are moderately manifested. Improvement comes gradually, the body temperature is reduced timetable, i.e. not immediately, but within a few days.

For pneumonia it is necessary complex of pathogenetic factors: A certain way of infection is a violation of the protective mechanisms of respiratory tract and the weakening of the immunological protective forces of the body.

Predisposing factors May be: perinatal pathology, unfavorable premorbid background (rickets, anemia, chronic nutritional disorders), vices of the heart and lungs, pathology of respiratory organs, repeated ARVI, hereditary diseases, bad socio-domestic conditions, etc.

3 ways of penetration of pneumonia penetration agents are possible into lungs: Aerogenic (bronchogen), hematogenic and lymphogenic (from the adjacent section of the lung tissue). Most often in the lower respiratory tract, the microflora from the nose and oral bodies falls into the aspiration of large quantities of the contents of the rotogling in patients without consciousness, with a violation of the act of swallowing, with a weakening of the cough reflex.

Aerogenic infection - hit in bronchioles or alveolar sputum particles containing infectious "Embol", which is facilitated by impaired mucocyllure clearance under the influence of ARVI or other reasons.

Viral infection contributes to the suppression of neutrophil functions, macrophages and T-lymphocytes, reducing the function of the local bronchopulmonal protection system.

Hematogenic pneumonia It is observed when "septic emblems" in the vein of a large circle of blood circulation. This pneumonia is secondary and occurs in children having acute or chronic foci of infection on the background of an adverse premorbide background (dysbacteriosis, candidiasis, acute intestinal infection).

Lymphogenicthe spread of infection is discount. However, from the pulmonary focus, the infection often passes on the lymphatic paths on the pleura.

Human respiration organs have a powerful protection system, which is represented by anatomical barriers for moving air flows, mucocyllary clearance, a number of reflector mechanisms, antibodies belonging to various classes of immunoglobulins, iron-containing proteins (lactoferrin and transferin), surfactant, alveolar macrophages, polymorphic leukocytes.

The overwhelming majority of microorganisms that have fallen into the respiratory tract, normally removed as a result of the functioning of the mukiciliary clearance - the first link of the protective mechanisms of the bronchial tree. The clearance is optimal with high elasticity and low viscosity of mucus.

However, slowing down the frequency or violation of the rhythm of ciliations, the change in the amount of mucus and / or its rheological properties create favorable conditions for persistence, aggregation and reproduction of bacteria. Muzin surrounding the accumulation of bacteria, in the absence of normal mukiciliary clearance, instead of a protective function begins to have a negative effect. It prevents the penetration of antibodies and antimicrobial factors, it makes it difficult to phagocytosis of microorganisms, thereby favorable infection and the development of pneumonia. Microbial agents have an independent ability to stimulate the hyperplasia of glassworm cells and the hypersecretion of mucus, as well as to cause the slowdown of the ciliations, disrupting the coordination of their movements up to a complete stop and even destruction of ciliary cells.

Influenced by infection in Alveoloch, inflammation is developing, which is distributed through the interlimoolar pores to other lung departments. Sensitization is developing to the infectious agent and an allergic reaction occurs, accompanied by the formation of immune complexes, interacting them with complement and the release of inflammation mediators.

At the heart of the development of pneumonia lie rapidly increasing oxygen deficiency (hypoxhemia) and the disruption of tissue respiration (hypoxia), which are a consequence of the rhythm disorders and the depth of breathing, a sharp decrease in gas exchange in lung tissue. Hypoxia progresses due to hemodynamic disorders, as well as developing anemia, violation of the function of the liver, hypovitaminosis, etc.

Immunological aspects of pneumonia. It is known that the complement system has a powerful antibacterial and antiviral activity, participates in the elimination of microbial and tissue antibodies and circulating immune complexes from the body, and is also able to activate specific immune reactions. In addition, the fragments of the components of the activated complementary stage have a pronounced pro-inflammatory effect. Complement activation products, like hormones and mediators of the immune system, mobilize and stimulate the vital activity of a plurality of organism cells that have receptors to the corresponding components of the complementary cascade. Due to this, the Complement system acts as an intermediary between the non-specific and specific links of the organism's immunobiological reactivity, between the immune, kininic and coagulation system of blood.

In the microcirculation system, pronounced changes occur, manifested by increased tissue permeability, blood concentration and increased aggregation of platelets. The peroxidation oxidation of lipids and the release of free radicals, damaging the pulmonary fabric, thereby aggravating neuro-trophic disorders in bronchops and lungs.

The main links of Pathogenesis of Pneumonia:

Penetration of the pathogen into the pulmonary tissue in combination with a violation of the system of local bronchopulmonal protection (reducing the function of cell and humoral immunity systems);

Development of local inflammatory process at the site of the deployment of the pathogen followed by generalization;

The occurrence of sensitization to infectious agents and the development of immune-inflammatory reactions;

Disorder of microcirculation in the lungs after the development of ischemia;

Activation of lipid peroxidation and proteolysis in lung tissue, leading to the development of the inflammatory process in alveoli and bronchiola.

Pneumonia - acute infectious inflammatory disease of the lungs with the involvement of all structural elements of lung tissue with the obligatory lesion of the alveoli and the development of inflammatory exudation in them.

Epidemiology: The incidence of acute pneumonia 10.0-13.8 per 1.000 population, among individuals\u003e 50 years - 17 to 1.000.

AtIology:

A) community-acquired (extractive) pneumonia:

1. Streptococcus Pneumoniae (Pneumococcus) - 70-90% of all patients with community-hospital pneumonia

2. Haemophilus influenzae (hemophilic chopstick)

3. Mycoplasma Pneumonaiae.

4. Chlamydia Pneumoniae.

5. Legionella Pneumophila.

6. Other pathogens: Moraxella Catarralis, Klebsiella Pneumoniae, Esherichia Coli, Staphylococcus Aureus, Streptococcus Haemoliticus.

B) Non-community (hospital / nosocomial) pneumonia (i.e. pneumonia, Developing 72 hours after hospitalizationIn the exception of infections that were in the incubation period at the time of the patient's arrival in the hospital And up to 72 hours after discharge):

1. Gram-positive flora: Staphylococcus aureus

2. Gram-negative Florama: Pseudomonas Aeruginosa, Klebsiella Pneumoniae, Escherichia Coli, Proteus Mirabilis, Haemophilus Influenzae, Enterobacter, Serratia

3. Anaerobic flora: gram-positive (peptostreptococcus, etc.) and gram-negative (Fusobacterium, Bacteroides, etc.)

Patient influence on etiology and the nature of the flow of hospital pneumonia has Specificity of the medical institution.

C) pneumonium in immunodeficiency states (congenital immunodeficiency, HIV infection, yathedral immunosuppression): Pneumocists, pathogenic mushrooms, cytomegaloviruses.

Factors predisposing to the development of pneumonia:

1) Violation of the interaction of the upper respiratory tract and esophagus (alcoholic sleep, anesthesia with intubation, epilepsy, injuries, strokes, gastrointestinal diseases: cancer, esophageal stricture, etc.)

2) Light and chest diseases with a decrease in local respiratory protection (fibrosis, kifoscolyosis)

3) infection of sinus sinuses (frontal, geimorov, etc.)

4) Secret-boating organism Factors (alcoholism, Uremia, SD, hypothermia, etc.)

5) immunodeficiency states, treatment with immunosuppressants

6) Travel, contact with birds (chlamydial pneumonia), air conditioning (legionellular pneumonia)

Pathogenesis of pneumonia:

1. Penetration of pathogens of pneumonia in respiratory departments of the lungs Bronchogenic (most frequently), hematogenic (during sepsis, endocardius of a three-grained valve, septic thrombophlebitis of pelvic veins, general infectious diseases), Per Continuinatem (directly from neighboring affected organs, for example, with liver abscess), lymphogenic paths with subsequent adhesion on the epithelial cells of the bronchopulmonal system . At the same time, pneumonia develops only in violation of the function of the system of local bronchopulmonal protection, as well as with a decrease in the overall reactivity of the organism and non-specific protection mechanisms.

2. Development under the influence of the infection of the local inflammatory process and its distribution on the pulmonary fabric.

PART OF MICROGANIMS (PNEMOKOKK, KLEBSELLA, EURTAINE WALK, HEMOFLY WALD) produce substances that increase vascular permeability, as a result of pneumonia, starting from a small hearth, further spreads through the lung tissue in the form of an "oil spots" through the alveolar pores of the KONA. Other microorganisms (staphylococci, a cinema stick) isolated exotoxins that destroy the pulmonary tissue, as a result of which the centers of necrosis are formed, which, merging, form abscesses. The production of cytokine leukocytes (IL-1, 6, 8, etc.), which stimulate chemotaxis macrophages and other effector cells plays a major role in the development of pneumonia.

3. Development of sensitization to infectious agents and immuno-inflammatory reactions (With a hyperergic reaction of the body, pneumonia is developing, with normo or hypergic - focal pneumonia).

4. Activation of lipid peroxidation and proteolysis in pulmonary fabricproviding a direct damaging effect on the pulmonary tissue and contributing to the development of the inflammatory process.

Classification of pneumonia:

I. etiological groups of pneumonia

II. Epidemiological groups of pneumonia: non-hospital (community-hospital, domestic, outpatient); hospital (nosocomial, nosocomial); atypical (i.e., caused by intracellular pathogens - legionells, mycoplasmas, chlamydia); Pneumonia in patients with immunodeficiency states and on the background of neutropenia.

III. Localization and length: one-sided (total, share, polistery, segmental, central (roar) and bilateral.

IV. By severity: severe; middle severity; Easy or abortive

V. According to complications (pulmonary and extlica): complicated and uncomplicated

Vi. Depending on the phase of the disease: height, resolution, reconvalue, protracted flow.

The main clinical manifestations of pneumonia.

A number of clinical syndromes of pneumonia can be distinguished: 1) intoxication; 2) general emphasis; 3) inflammatory changes in pulmonary fabric; 4) lesions of other organs and systems.

1. Pulmonary manifestations of pneumonia:

A) Cashel - at first dry, many in the first day in the form of frequent passing, on the 2nd day the cough with a hard-leaving mocrium-purulent wet; Patients with equity pneumonia often appear "rusty" the sputum in connection with the appearance of a large number of erythrocytes in it.

B) chest pain - the most characteristic of equity pneumonia is due to the involvement in the process of pleura (pleuropneumonia) and the lower intercostal nerves. The pain appears suddenly, it is quite intense, enhanced with cough, breathing; With a pronounced pain, there is a lag of the corresponding half of the chest in the act of breathing, the patient "spreads it" and holds the hand. With focal pneumonia, pain can be weakly pronounced or absent.

C) Dyshka - its severity depends on the length of pneumonia; With equity pneumonia, significant tachipne may be observed up to 30-40 minutes, the face is pale, looked, with inflating nose with breathing. Dyspnea is often combined with the feeling of "plow in the chest".

D) physical signs of local pulmonary inflammation:

1) dulling (shortening) of the perfume sound, respectively, the localization of the inflammatory hearth (always clearly determined with the equity and not always expressed during focal pneumonia)

3) Capital, listening above the hearth focus - resembles a small crackling or sound, which is suspended if the hair beam is riveted with fingers; due to a sprawling during the inspire of the walls of the alveoli, impregnated with inflammatory exudate; Lisvat only during the inhalation and not heard during the exhalation

For the start of pneumonia, Crepitatio Indux is characterized, it is a quiet, listened to a limited area and as if it comes from afar; To resolve pneumonia, Crepitatio Redux is characterized, it is loud, sonorous, is heard on a more extensive area and, as it were, directly above the ear. In the midst of pulmonary inflammation, when the alveoli is filled with inflammatory exudate, the attitudes are not auditioned.

4) Melchopusarious wheezes in the projection of the focus of inflammation - are characteristic of focal pneumonia, are a reflection of the accompanying bronchopneumonia of local bronchitis

5) Change of vesicular breathing - in initial stage And the pneumonia permission phase vesicular breathing is weakened, and with the equity pneumonia in the phase of a pronounced compaction of the pulmonary tissue, vesicular breathing is not auditioned.

7) Bronchial breathing - listened to the presence of an extensive section of the sealing of lung tissue and preserved bronchial conductivity.

8) Spit friction noise - determined in pleuropneumonia

2. Empty manifestations of pneumonia:

A) fever, octvinations - Pneumonia begins acutely, intensive pain in the chest, increasing in respiration, is observed, increasing temperatures up to 39 ° C and higher; The focal pneumonia begins gradually, the increase in temperature is gradual, as a rule, not higher than 38.0-38.5 ° C, chills are not natural.

B) intoxication syndrome - general weakness, reduction of working capacity, sweating (more often at night and with insignificant exercise), reduction or complete absence of appetite, Malgia, arthritia at the height of fever, headache, with a severe current - confusion of consciousness, nonsense. With a serious flow of equity pneumonia, jaundice is possible (due to the violation of the liver function with severe intoxication), short-term diarrhea, proteinuria and cylindruria, herpes.

Diagnosis of pneumonia.

1. Radiography of the organs of the chest - The most important method of diagnosing pneumonia.

In the initial stage of pneumonia - the strengthening of the pulmonary pattern of the affected segments.

In the seal stage, the intensive dimming of the lung sections covered by inflammation (parts of the infiltration of lung tissue); with equity pneumonia shadow uniform, homogeneous, in central Department More intense, in focal pneumonia inflammatory infiltration in the form of individual foci.

In the resolution stage, the size and intensity of inflammatory infiltration decrease, gradually it disappears, the structure of the lung fabric is restored, but the root of the lung for a long time May remain expanded.

2. Laboratory inflammation syndrome: leukocytosis, leukocytic formula, to the left, toxic grit neutrophil, lymphopenia, eosinopenia, increasing ECD in the UAC, increase the content of A2 and G-globulines, sialic acids, serumcoid, fibrin, haptoglobin, LDH (especially the 3rd fraction), reactive protein into the tank.

Criteria for the severity of the flow of pneumonia.

	Severity
	Not more than 25.		40 or more
			40o and above
Hypoxemia	There is no cyanosis	Nonweight cyanosis	Pronounced cyanosis
		Unwatched	Displays
Extensive defeat	1-2 segments	1-2 segments from two sides or a whole share	More than 1 share, total; Polycegimentary

Comparative characteristics of equity and focal pneumonia.

Signs	Pneumonia	Heat pneumonia
Beginning of the disease	Acute, sudden, with high body temperature, chills, chest pains	Gradual, as a rule, after or on the background of respiratory viral infection
Inxication syndrome	Expressed significantly	Weakly expressed
	Painful, first dry, then with the separation of "rusty" sputum	As a rule, painless, with the separation of mucous-purulent sputum
Chest pain	Characteristic enough intense associated with breathing, cough	Little-accurate and non-intense
	Very characteristic	Little Calibric
Bottle of percussion sound above the lesion zone	Very characteristic	It is not always observed (it depends on the depth of the location and the size of the inflammatory hearth)
Ascriptive picture	Capitation at the beginning of inflammation and in the permission phase, bronchial breath in the phase of the disease of the disease, often the noise of friction of the pleura	At a limited area, attitudes are determined, the weakening of vesicular breathing, listened to the small-pushed wheezes
Dyspnea and cyanosis	Characteristic	Little pronounced or missing
Laboratory signs of inflammation	Expressed clearly	Less than expressed
X-ray manifestations	Intense homogeneous darkening of lung share	Spotted focal blackout of various intensities (in the area of \u200b\u200bone or several segments)

Complications of pneumonia.

1. Little: but. Parapnemonic pleurisy b. Abscess and gangrene lung in. Bronchial obstruction syndrome. Acute respiratory failure.

2. Outlogochny: but. acute pulmonary heart b. Infectious toxic shock in. Non-specific myocarditis, endocarditis G. Meningitis, Meningoencefalitis d. DVS-syndrome E. Psychosians. anemia z. Acute glomerulonephritis and. Toxic hepatitis

Basic principles of pneumonia treatment.

1. Therapeutic regime: Hospitalization (outpatiently treated only notifying pneumonia with proper care for the patient).

During the entire feverish period and intoxication, as well as before the elimination of complications - bedding, after 3 days after the normalization of body temperature and the disappearance of intoxication - semi-noise, then the steamed mode.

Need proper care for the patient: a spacious room; good lighting; ventilation; Fresh air in the ward; Careful mouth care.

2. Healing nutrition: In the acute fevering period, abundant drink (cranberry juice, fruit juices) about 2.5-3.0 liters per day; In the first days - a diet from easily absorbed products, compotes, fruits, in the subsequent - table number 10 or 15; Smoking and alcohol are prohibited.

3. Etiotropic treatment: AB is the basis for the treatment of acute pneumonia.

Principles of etiotropic therapy of pneumonia:

A) treatment should begin as soon as possible before the selection and identification of the pathogen

B) treatment should be carried out under clinical and bacteriological control with the determination of the pathogen and its sensitivity to

B) AB should be appointed in optimal doses and with such intervals to ensure the creation of the medical concentration in the blood and pulmonary fabric

D) AB treatment should continue before the disappearance of intoxication, normalizing the body temperature (at least 3-4 days later than normal temperature), physical data in the lungs, resorption of inflammatory infiltration in the lungs according to x-ray research.

E) In the absence of the effect of AB for 2-3 days, it change it, with a severe flow of pneumonia AB combined

E) unacceptable an uncontrolled application of AB of funds, since the virulence of infection pathogens is increasing and the form-resistant form arises

G) with prolonged use of AB, the lack of vitamins of the group is as a result of a violation of their synthesis in the intestines, which requires the correction of vitamin imbalance; It is necessary to diagnose candidomicosis and intestinal dysbiosis in time, which may develop in the treatment of ab

H) In the course of treatment, it is advisable to control the indicators of the immune status, since the treatment of AB may cause oppression of the immunity system.

Algorithm of empirical antibiotic therapy of community-hospital pneumonia (patient's age up to 60 years): ampicillin (better amoxicillin) 1.0 g 4 times a day, if there is an effect - continue therapy to 10-14 days, if not - assign options: erythromycin 0.5 g 4 times a day / doxycycline 0.1 g 2 Once a day / Biseptol 2 tablets 2 times a day for 3-5 days, if there is an effect - continue therapy to 10-14 days, if not - hospitalization in hospital and rational antibiotic therapy.

Algorithm of empirical antibiotic therapy of the community-friendly secondary pneumonia (the age of the patient is over 60): Cefalosporins II II generations (cefaclor, cefuroxime) orally or per / m for 3-5 days, if there is an effect - continue therapy 14-21 days, if not - assign options: erythromycin 0.5 g 4 times a day; Sumamed 0.5-1.0 g per day for 3-5 days; There is an effect - continue therapy 14-21 days, there is no effect - hospitalization and rational antibiotic therapy.

4. Pathogenetic treatment:

A) restore the drainage function of the bronchi: Expectaurant (bromgexine, ambroxol / lazolvan, bronchikum, licorice root 5-7 days), Mulcolitis (acetylcysteine \u200b\u200bfor 2-3 days, but not from the 1st day); With a serious course of the disease - sanitation bronchoscopy with 1% dioxidine solution or 1% Furagin solution.

B) normalization of the tone of bronchial muscles: In the presence of bronchospasm, bronchodilators are shown (Ehufillin in / in drip, prolonged theophyllins inward, aerosol B2-adrenomimetics).

C) immunomodulatory therapy: Prodigiosan in gradually increasing doses from 25 to 100 μg in / m with an interval of 3-4 days, course 4-6 injections; T-activin 100 μg 1 time in 3-4 days p / k; Timalin at 10-20 mg per / m 5-7 days; sodium nucleinate 0.2 g 3-4 times a day after meals; Levamizol (decaris) of 150 mg 1 time per day for 3 days, then 4 days break; The course is repeated 3 times; Adaptogens (Eleutherococcus extract 1 teaspoon 2-3 times a day; Ginseng tincture of 20-30 drops 3 times a day; The tincture of the Chinese lemongrass is 30-40 drops 3 times a day; interferon preparations (1 MP contents are dissolved in 1 ml Isotonic sodium chloride, introduced in / m for 1 million meters 1-2 times a day daily or every other day within 10-12 days).

D) antioxidant therapy: Vitamin E 1 capsule 2-3 times a day inside 2-3 weeks; Essentialy 2 capsules 3 times a day during the entire period of the disease; Emoxipin 4-6 MK / kg / day V / in drip on the saline.

5. Fighting intoxication: in / in drip hemodez (400 ml 1 time per day), isotonic solution of sodium chloride, 5% glucose solution; Abundant drinking cranberry morse, fruit juices, mineral Water; With pronounced intoxication - plasmapheresis, hemosorption.

6. Symptomatic treatment:

A) antitussive tools: prescribe in the first days of the disease at dry cough (Liebeksin 0.1 g 3-4 times a day, Tusuprex at 0.01-0.02 g 3 times a day).

B) antipyretic drugs and painful agents, anti-inflammatory drugs (paracetamol 0.5 g 2-3 times a day; Voltaren 0.025 g 2-3 times a day)

7. Physiotherapy, LFK, respiratory gymnastics: Inhalation therapy (bioparox every 4 hours 4 inhalation per inhalation; anti-inflammatory chamomile beams, Hypericum in the form of inhalation; acetylcysteine); electrophoresis calcium chloride, potassium iodide, lidases, heparin to the area of \u200b\u200bthe pneumonic focus; Electrical field UHF in a low-imparal sheet dose, inductothermia, microwave on a smoking hearth; Applications (paraffin, ozokerite, mud) and needleflexotherapy in the pneumonia permission phase; LFK (in the acute period - the treatment of the situation, the patient should lie on a healthy side 3-4 times a day to improve the aeration of the patient of the lung, as well as on the abdomen to reduce the formation of pleural adhesions; static breathing exercises with the subsequent connection of exercises for limbs and torso, training of diaphragmal respiration); Ground massage.

8. Sanatorium-smokery and rehabilitation.

With nongendling fine-fought pneumonia, the rehabilitation of patients is limited to treatment in the hospital and observation in the clinic. Patients with transmitted common pneumonia with severe intoxication, hypoxemia, as well as persons with a sluggish flow of pneumonia and its complications are sent to the rehabilitation center (separation). Patients who have suffered pneumonia are sent to local sanatoriums (Belarus »Minsk region," Bug "," Alesya "of the Brest region) and on climatic resorts with a dry and warm climate (Yalta, Gurzuf, South of Ukraine).

ITU: Approximately the validity period in the mild form of acute pneumonia 20-21 days; with a moderate form of 28-29 days; With severe form, as well as with complications: 65-70 days.

Dispensarization: patients who have suffered pneumonia and writing with clinical recovery, there are 6 months with surveys after 1, 3 and 6 months after discharge from the hospital; Patients who suffered pneumonium with a protracted flow, discharged with residual clinical manifestations of the disease, are observed 12 months with surveys after 1, 3, 6 and 12 months.

Pneumonia- acute or chronic diseases characterized by the inflammation of parenchyma and (or) interstitial tissue of the lungs. Most of the sharp pneumonia are parenchymal or predominantly parenchymal and are divided into bruboral (equity) and ocher (slices). Controversial selection of acute interstitial pneumonia. Chronic pneumonia, on the contrary, is largely associated with the lesion of the interstitial tissue of the lungs and only in the period of exacerbation are distributed to the lung parenchyma.

Etiology and pathogenesis of pneumonium. Polyethological diseases arising from the impact on the pulmonary tissue of various bacteria (pneumatic, stafilo and streptococci, Chlebseyella pneumonia, influenza wand, sometimes intestinal wand, protein and a blue chopstick, causative agent of Ku-fever - Ricketsia Berenet) and their toxins, some viruses, Mycoplasma pneumonia, mushrooms. In the emergence of sharp pneumonia, viral-bacterial associations play an important role. Chemical and physical agents - Impact on the lungs chemical substances (gasoline, etc.), thermal factors (cooling or burns), radioactive radiation - as etiological factors are usually combined with infectious. Pneumonia can be a consequence of allergic reactions in the lungs or manifestation of systemic disease (interstitial pneumonia during collamines).

The pathogens penetrate into the pulmonary tissue with bronchiogenic, hematogenic and lymphogenic paths, as a rule, from the upper respiratory tract, usually if there is sharp or chronic foci of infection and infectious foci in bronchops (chronic bronchitis, bronchiectase). Violations of various protective mechanisms of the bronchopulmonary system and the state of humoral and tissue immunity of the body play an important role in the pathogenesis. The survival rate of bacteria in the lungs, their reproduction and distribution according to Alveolums largely depend on their aspiration with mucus from the upper respiratory tract and bronchi (which is favored by cooling), from excessive formation of the edema, covering the pneumonia with a traveler (pneumococcal) lungs. At the same time, immunological damage and inflammation of the pulmonary tissue are possible due to the reactions to the antigenic material of microorganisms and other allergens. Viral infection by itself, causing inflammation of the upper respiratory tract and bronchi, and in some cases - and pneumonia, more often favors the activation of bacterial infection and the occurrence of bacterial focal or equity pneumonia. The appearance of bacterial pneumonias usually at the end of the 1st or early 2nd week of respiratory viral disease corresponds to a significant decrease in the bactericidal activity of the alveolar-macrophage lung system. Chronic pneumonia arises as a consequence of unresolved acute pneumonia as a result of slowing down and stopping the resorption of the exudate in alveoli and the formation of pneumosclerosis, inflammatory-cell changes in the interstitial tissue, often immunological character (lymphocyte and plasmocycle cell infiltration). Immunological disorders under the influence of repeated respiratory viral infection, chronic infection of the upper respiratory tract (chronic tonsillites, sinuits, etc.) and bronchi, under the influence of metabolic disorders in chronic alcoholism, under the influence of metabolic disorders in chronic alcoholism, diabetes, etc.).

Symptoms and Pneumonia depend on the etiology (usually the species of the pathogen), the nature and phases of the flow, the morphological substrate of the disease and its prevalence in the lungs, as well as complications (pulmonary suppuration, pleurisy, etc.). Truck (pneumococcal) Pneumonia usually begins acutely, often after cooling: the patient is experiencing a stunning chill, the body temperature rises to 39 - 40 ° C, less often up to 38 or 41 ° C, worried pain in breathing on the side of the affected lung; They are enhanced by cough, first dry, later with the "rusty" or purulent viscous wet with an admixture of blood. A similar or not so violent launch of the disease is possible in the outcome of a sharp respiratory disease or against the background of chronic bronchitis. The patient's condition is usually heavy. Skin Covers Persons hyperemic and cyanotic. Breathing from the very beginning of the disease is a rapid, superficial, with inflating the wings of the nose. It is often marked by Herpes Labalis et Nasalis. Before applying antibacterial therapy heat held on average week, declining sharply ("critically"); under influence antibacterial drugs There is a gradual ("Lithic") temperature decrease. The chest is lagging behind in the act of breathing on the side of the affected lung, the percussion of which, depending on the morphological stage of the disease, is detected by a dull thympanite (stage of the tide), shortening (dull) of the pulmonary sound (stage of red and gray compensation) and the pulmonary sound (resolution stage). With auscultation, depending on the stadium nature of morphological changes - revealed reinforced vesicular respiration and Crepitatio indux, bronchial breathing and vesicular or weakened vesicular breathing, against which Crepitatio Redux is suspended. In the phase of the comrades, reinforced voice trembling and bronchophony are determined. Due to the unevenness of the development of morphological changes in the lungs, the percussion and auction paintings can be the motley. Due to the defeat of the pleura (parapneumonic serofibrinous pleurisy), the noise of friction of the pleura is listened. In the midst of the disease, the pulse rapid, soft, corresponds to a reduced blood pressure. Frequently mute i tone and accent II Tone on pulmonary artery. It is characterized by neutrophilic leukocytosis (1.2-104 - 1.5 * 104 in 1 μl), occasionally hyperlaccitosis (up to 3.0-104 in 1 μl). The absence of leukocytosis can be a prognostically unfavorable sign. Education ESP. For x-ray study A homogeneous dimming of the entire affected share or its part is determined, especially on lateral radiographs. Radioscopy may be insufficient in the first hours of the disease.
Atypical flow of pneumonia More often observed in individuals suffering from chronic alcoholism. Similarly, the pneumococcal can occur the share staphylococcus pneumonia. More often, however, it flows more hard, accompanied by the destruction of the lungs with the formation of thin-walled air cavities, lung abscesses. With the phenomena of pronounced intoxication proceeds staphylococcus (usually polydolash) pneumonia complicating viral infection Bronchildren system (viral-bacterial pneumonia). This pneumonia usually leads to a patient to a rapid fatal outcome. The difficult flow is also observed in the lobar pneumonia caused by Klebsiella Pneumonia (Fredeland's chopstick); It occurs relatively rarely (more often in alcoholics), leads to high mortality (up to 50%), requires early diagnosis. It is characterized by the left spread with more frequent than with pneumococcal pneumonias, involving the upper fractions. The sputum is often jelly, viscous, but can be purulent or rusty. Typically, the formation of abscesses and complication of the empire.

Focal pneumonia, or bronchopneumonia, arise as complications of sharp or chronic inflammation upper respiratory tract and bronchi in patients with stagnant lightweight, heavy, depleting organism diseases, in postoperative period. The disease can begin with chills, but not so pronounced as with a bruboral pneumonia. The body temperature rises to 38-38.5 ° C, less often above. A cough, dry or with mucous-purulent sputum appears or enhanced. Pain in the chest with cough and inhale. With drain focal pneumonia, the condition worsens: pronounced shortness of breath, cyanosis; There is a shortening of a pulmonary sound, breathing can be enhanced vesicular with the foci of bronchial, the foci of fine and medium-repeated wheezes are listened, attitudes. Often there is a "stern" of the clinical picture of the disease. For viral, kricricketsome and mycoplasma pneumonia, the discrepancy between pronounced intoxication (fever, head and muscle pain, sharp malaise) and the lack of or weak severity of the symptoms of the defeat of the respiratory organs. On the radiograph (sometimes only on the tomogram), lolk, subsegimentary and segmental shadows, enhancement of the pulmonary pattern are detected. Common and drain focal, especially staphylococcal, pneumonia are accompanied by neutrophilic leukocytosis, increased SEE. Viral, rickettsiosis and mycoplasma pneumonia are usually not accompanied by leukocytosis, sometimes leukopenia is expressed. Hemorrhagic influenza pneumonia is particularly difficult, usually viral-staphylococcal: pronounced intoxication, hemoptail, severe respiratory failure, hemodynamic disorders. In patients with ornithous pneumonia, hepatolyenal syndrome is possible.

Chronic pneumonia, being limited (segment, share) or widespread inflammation of the bronchology system, is clinically characterized by a wet cough for many months (sometimes many years), the shortness of breath first during exercise, further alone, often expiratory character (astmoid syndrome), periodic amplification These symptoms, accompanied by an increase in body temperature, chest pains, not always shortening the pulmonary sound, but usually amplifying vesicular respiration, the presence of dry and solid-caliber wet wheezes, attitudes. Changes in physical research are exacerbated with the development of emphysema (box sound, weakened breathing), bronchiectasis (resistant foci of wet wheezes), sometimes chronic abscess (amphoric breathing, large-tested wet wets). The aggravation of the disease can manifest itself with neutrophilic leukocytosis, an increase in ESP, acutely phase reactions (an increase in sialic acids, an increase in C-reactive protein, disproteinemia, etc.). With radiographic, bronchon and bronchoscopic studies, the foci of pneumonic infiltration (the period of exacerbation) are combined with the fields of pneumosclerosis, inflammation and deformation of the bronchi, less often with their expansion (bronchiectase) and the presence of cavities in the parenchyma (abscess).

Frequent complication of pneumonium - exudative pleurisy.It is usually poorly expressed and has no clinical value. With an increase in the exudate, its suppuration acquires the leading knowledge in the clinical picture (see Puritism, as well as emphasis in the chapter "Surgical Diseases"). Heavy complication is the abscess of the lungs (see Abscess in the chapter "Surgical Diseases"). Staphylococcus lung destruction can be complicated by the breakdown of the cavity and the development of spontaneous (custom-only valve) pneumothorax or popenemotrax. Among the extravalous complications are the most important vascular (collapse) and heart failure. They occur in patients with the common (usually multi-column) process at late hospitalization and non-efficiency treatment, often on the background chronic diseases Cardiovascular system (ISH-MICHICAL DISEASE AND CAPTERS OF THE CAPTER, HYPERTIYA). Acute pneumonia can be complicated by focal jade, significantly less often - diffuse glomerulonephritis. The lesion of the liver during the lobar pneumonia can manifest a jaundice, which may be a consequence of hemolytic immune anemia, in particular with mycoplasma pneumonia. Rare complications were pericardits, endocardits, meningitis.

Diagnostics take into account that shortening of the percussion sound with focal pneumonias are usually no, but there is a strengthening of vesicular breathing, sometimes with the foci of bronchial, attitudes, fine and medium-bubblers, focal blackouts, better detectable on X-ray grams (sometimes on tomograms). To establish a etiological diagnosis Before starting treatment, a spruder or strokes from a pharynx, larynx (and sometimes washed from larynx and bronchi) on tank terriah, including mycobacterium tuberculosis, viruses, Miko Plasma Pneumonia and Ricketsia. It is possible to assume viral or ricketsiotic etiology of the disease by inconsistency between acutely emerging infectious-toxic phenomena and minimal changes in the respiratory organs with a direct study (focal or interstitial shadows in the lungs are detected.

In the differential diagnosis of acute and chronic pneumonia, carefully assembled history is crucial, with chronic pneumonia, indicating in the past in the past, pneumonia, frequent "outbreaks" of pulmonary symptoms (cough, wet, shortness of breath), and radiologically detected pneumosclerosis. For acute bronchitis And the exacerbation of chronic bronchitis, in contrast to pneumonia, intoxication is less pronounced, x-ray does not detect the foci of dimming. With the complication of chronic bronchitis of the bronchopneumonia, the permission of pneumonia (but not always bronchitis!) Under the influence of treatment, should be regarded as evidence of the undergoing acute pneumonia; On the contrary, steadyly determined physical symptoms and peribroscopic pneumosclerosis should be regarded as evidence of the aggravated aggravation of chronic pneumonia.

The beginning of tuberculous exudative pleurite can be as sharp as pneumonia, shortening of the percussion sound and bronchial breathing over the region collaborated to the root of the lung can imitate signs of equity pneumonia. Errors can be avoided with a thorough percussion that detects a bowl of dull sound and loose breathing (with an em-pita - weakened bronchial breathing!). Differentiations helps a radiograph in the Boko-Military Projection (intensive shadow in the axillary region) and pleural puncture with the subsequent study of the exudate. In contrast to neutrophilic leukocytosis with the equity (less often the focus) pneumonia, white blood with an exudative pleurite of tuberculosis etiology is usually not changed. In contrast to equity and segmental pneumoniums with tuberculosis infiltrate or focus-in tuberculosis, it is usually less acute start; Pneumonia under the influence of nonspecific therapy is permitted in the next 11-12 weeks, while the tuberculosis process does not give in so quickly even tuberculostatic therapy.

Severexication with high fever with weakly pronounced physical symptoms is characteristic of miliary tuberculosis, which contributes to its differentiation with small-scale common pneumonia. Acute pneumonia and obstructive pneumonitis at bronchogenic cancer can begin sharply against the background of apparent well-being, often after cooling, chills, fever, pain in the chest, are observed, but the cough with obstructive pneumonite is often dry, parotid, and later with a separation of a small amount of sputum and hemoptia; In obscure cases, only bronchoscopy allows you to refine the diagnosis.

Directory of a practical doctor / ed. A. I. Vorobyva. - M.: Medicine, 1982