Pulmonary infiltration syndrome in children. Infiltration of lung tissue. Reasons for the development of pathology

Definition. Etiology and pathogenesis. Morphology.
Pulmonary infiltration syndrome consists of characteristic morphological, radiation and clinical manifestations. In practice, this syndrome is most often diagnosed on the basis of clinical and radiological data.

A morphological (bioptic) examination is carried out if a more in-depth examination of the patient is necessary. Pathologically, pulmonary infiltration refers to the penetration into lung tissue and the accumulation of cellular elements, fluids and various chemicals in them. Impregnation of lung tissues only with biological fluids without admixture of cellular elements characterizes pulmonary edema, and not infiltration.

The main diseases that cause pulmonary infiltration syndrome:

In pathology, lung infiltration of inflammatory origin is most common. Inflammatory infiltration of the lungs can be leukocyte, lymphoid (round cell), macrophage, eosinophilic, hemorrhagic, etc. An important role in the formation of the inflammatory infiltrate also belongs to other components of the connective tissue - the interstitial substance, fibrous structures.

Leukocyte inflammatory infiltrates are often complicated by suppurative processes (for example, lung abscess), since proteolytic substances that appear during the release of lysosomal enzymes of polymorphonuclear leukocytes often cause melting of infiltrated tissues. Loose, rapidly occurring (for example, acute inflammatory) infiltrates usually resolve and do not leave noticeable marks. Infiltration with significant destructive changes in the lung tissue in the future most often produces persistent pathological changes in the form of sclerosis, decreased or loss of lung function.

Lymphoid (round cell), lymphocytic-plasma cell and macrophage infiltrates in most cases are an expression of chronic inflammatory processes in the lungs. Against the background of such infiltrates, sclerotic changes often occur. The same infiltrates can be a manifestation of extramedullary hematopoietic processes, for example, lymphocytic infiltrates.

Lung tissues are infiltrated with hematopoietic cells. In such cases, they talk about tumor infiltration or ifiltrative tumor growth. Infiltration by tumor cells leads to atrophy or destruction of the lung tissue.

Symptoms pulmonary infiltration syndrome depend primarily on the disease that causes it, the degree of activity of the inflammatory process, the area and location of the lesion, complications, etc. The most typical general symptoms of pulmonary infiltration are cough, shortness of breath, and fever. If the focus of infiltration is located on the periphery of the lung and extends to the pleura, chest pain may occur when coughing and deep breathing. In the process of objective examination of patients, increased breathing rates and lag of the affected half of the chest in the act of breathing are often revealed. Percussion and auscultation data for small and deeply located foci of infiltration do not reveal deviations from the norm. In the presence of larger areas of pulmonary infiltration, especially those located on the periphery of the lung tissue, it is possible to determine dullness of percussion sound, vesiculobronchial or bronchial breathing, dry and moist rales, crepitus in a limited area of ​​the chest, and increased vocal tremors on the affected side.

Infiltration is characterized by a moderate increase in the volume of lung tissue and its increased density. Therefore, the radiation signs of pulmonary infiltration have their own characteristics. For example, inflammatory infiltration is characterized by an irregular form of darkening and uneven outlines. In the acute stage, the contours of the darkening are blurred, gradually moving into the surrounding lung tissue. Areas of chronic inflammation cause sharper, but also uneven and jagged contours. Against the background of the shadow of inflammatory infiltration of the lung, you can often find light branching stripes - these are the lumens of the air-filled bronchi.

Diagnostics. Clinic, radiation, laboratory, bacteriological and morphological methods.

Pulmonary infiltrate- an area of ​​lung tissue characterized by the accumulation of cellular elements usually not characteristic of it, increased volume and increased density.

According to X-ray data The chest organs are distinguished: a) limited darkening and foci; b) single or multiple rounded shadows; c) pulmonary dissemination; d) increased pulmonary pattern

Clinically: subjective symptoms are often non-specific (fatigue, decreased performance, headache, weight loss), shortness of breath, cough, sputum production, hemoptysis, chest pain indicate lung damage; objectively: lag of the diseased half of the chest in breathing, increased vocal tremor in the projection of the compaction, dull or dull percussion sound, bronchial breathing (large foci) or weakened vesicular (small foci), additional respiratory sounds - crepitation, various wheezing, pleural friction noise, etc. .

Pulmonary infiltrate is characteristic of the following diseases:

1. pneumonia– acute infectious inflammation of the lung tissue with mandatory involvement of the respiratory parts of the lungs in the process; characterized by an anamnestic connection with acute respiratory viral infection, contact with a patient, malaise, hyperthermia and other symptoms of general intoxication for several days, cough, chest pain, signs of respiratory failure

2. infiltrative tuberculosis– characterized by a gradual onset with a preceding period of unmotivated malaise, low-grade fever, cough, pulmonary infiltrate in the area of ​​the apex or upper lobe in the form of a uniform darkening with fresh foci in the adjacent tissue, a “path” to the root, calcified l. u. in the roots of the lungs

3. pulmonary eosinophilic infiltrate(local pulmonary eosinophilitis - simple pulmonary eosinophilitis and chronic eosinophilic pneumonia, pulmonary eosinophilitis with asthmatic syndrome, pulmonary eosinophilitis with systemic manifestations) - characterized by the absence of manifestations or a clinic similar to pneumonia, homogeneous infiltrates in various parts of the lungs of a “volatile” nature, rapid effect of GCS therapy

4. darkening in malignant tumors(central and peripheral lung cancer, single and multiple metastases to the lungs, lymphomas, lung sarcomas) - peripheral cancer is characterized by a history of long-term smoking, unproductive cough, repeated pneumonia of one localization, old age, on a plain radiograph the shadow is uniform or with decay cavities, with lumpy, uneven contours, the surrounding lung tissue is intact, l. u. the mediastinum is often enlarged; with metastases on the radiograph – multiple round shadows

5. darkening in benign tumors(hamartoma, bronchial adenoma, chondroma, neuromas) – single spherical formations with clear contours that exist for a long time; there is no “path” to the root; surrounding lung tissue is intact

6. lung development abnormalities: lung cyst with abnormal blood supply (intralobar sequestration of the lung); simple and cystic pulmonary hypoplasia; arteriovenous aneurysms in the lungs; lymphangiectasia and other abnormalities of the lymphatic system

7. suppurative lung diseases: lung abscess, lung gangrene

8. focal pneumosclerosis: post-pneumonic, post-tuberculosis

9. pulmonary infarction after pulmonary embolism– develops only in some patients who have undergone pulmonary embolism; diagnosis is based on a comparison of complaints, anamnesis, results of instrumental examination (ECG, chest X-ray, isotope lung scintigraphy, CT, angiopulmonography and spiral CT with contrast of the pulmonary artery)

10. pulmonary hemosiderosis– combined with hemosiderosis of other organs, characterized by repeated hemorrhages into the lung tissue, hemoptysis, anemia; on a plain X-ray of the chest - bilateral symmetrical small-focal changes in the lungs; hemosiderophages are found in sputum; lung biopsy required

11. pulmonary echinococcosis– there are no subjective symptoms, the cyst is round or oval with constrictions and protrusions, with smooth, clear contours, and a homogeneous structure; surrounding lung tissue is intact

12. pulmonitis in immunopathological diseases: systemic vasculitis, SLE, Goodpasture's syndrome, Wegener's granulomatosis, basal pneumofibrosis in systemic sclerosis

13. idiopathic pulmonary fibrosis(fibrosing alveolitis)

14. pulmonary sarcoidosis– often characterized by a gradual asymptomatic onset without signs of intoxication, erythema nodosum, radiographs characteristic of TB, but with negative tuberculin tests

15. drug-induced toxic pneumonia(nitrofurans, amiodarone, PAS, sulfonamides, salicylates)

16. foreign body aspiration

17. pneumoconiosis

18. alveolar proteinosis– accumulation of protein-lipoid substances in the alveoli and bronchioles; radiographically – “alveolar filling syndrome”; in the histology of lung tissue biopsy - a substance that gives a PAS-positive reaction

Source: uchenie.net

Causes

A common cause of infiltration in the lungs is pneumonia.

The main causes of lung infiltration are the following pathological conditions:

1. Pneumonia (bacterial, viral, fungal).
2. Tuberculosis process.
3. Allergic diseases (eosinophilic infiltrate).
4. Malignant or benign tumor.
5. Focal pneumosclerosis.
6. Pulmonary infarction.
7. Systemic connective tissue diseases.

The classic course of pulmonary infiltration syndrome is observed with pneumonia and involves a sequential change of three phases of the inflammatory process:

• alteration under the influence of damaging factors and release of biologically active substances;
• exudation;
• proliferation.

Clinical signs

The presence of infiltration in the lungs can be assumed in the presence of clinical signs:

• dullness of percussion sound over the affected area;
• increased vocal tremors, determined by palpation;
• weakened vesicular or bronchial breathing during auscultation;
• lag of the diseased half of the chest in the act of breathing (with extensive lesions).

Such patients may complain of shortness of breath, cough and pain in the chest (if the pleura is involved in the pathological process).

Differential diagnosis of pulmonary infiltrates

Identification of signs of infiltration of lung tissue prompts the doctor to conduct a diagnostic search. In this case, the patient’s complaints, medical history data, and the results of an objective examination are compared.

The first thing you should pay attention to is fever:

• If this is absent, then a nonspecific inflammatory process in the lungs is unlikely. This course is typical for pneumosclerosis or a tumor process.
• If there is fever, it may be pneumonia, a lung abscess in the infiltration stage, pulmonary infarction, a festering cyst, etc.

If any of these diseases is suspected, the specialist will refer the patient for a chest x-ray. This study allows not only to confirm the presence of infiltration by identifying an area of ​​“darkening” on an x-ray, but also to evaluate its size, shape and intensity.

If patients with infiltration syndrome do not have any health complaints and this pathology is detected during a routine X-ray examination, then its causes may be:

• pneumosclerosis;
• infiltrative tuberculosis;
• obstruction of the bronchus by a tumor.

In parallel with x-ray examination, other diagnostic methods are used in the process of differential diagnosis:

• clinical blood test;
• sputum examination;
• spirography;
• bronchoscopy;
• CT scan.

Diseases that occur with pulmonary tissue infiltration syndrome have their own characteristics, let's look at some of them.

Lung infiltration syndrome in lobar pneumonia

The disease begins acutely and progresses through 3 stages. Using his example, one can trace the classic course of pulmonary infiltration syndrome.

1. At the first stage, the alveoli swell, their walls thicken, become less elastic, and exudate accumulates in their lumen. Patients at this time are worried about a dry cough, fever, mixed shortness of breath, and weakness. Objectively, signs of infiltration of the lung tissue are detected (decreased elasticity of the lung tissue, dullness of percussion sound, weakened vesicular breathing, etc.). In this case, side respiratory sounds are heard in the form of crepitus “hot flashes”.
2. In the second stage of the disease, the alveoli are completely filled with exudate and the density of the lung tissue approaches the liver. The clinical picture changes: the cough becomes wet with rust-colored sputum, chest pain appears, shortness of breath increases, and a high body temperature persists. Bronchial breathing is heard over the affected area. During percussion, a more pronounced dullness of the percussion sound is determined.
3. At the third stage, the inflammatory process resolves, the exudate in the alveoli resolves, and air begins to flow into them. The patient's body temperature decreases, shortness of breath decreases, and a productive cough with mucopurulent sputum is disturbed. Over the lungs, weakened breathing, crepitus “ebb” and fine moist rales are heard.

It should be noted that the pathological process is often localized in the lower or middle lobes. 1-2 days after the start of antibacterial therapy, the patients’ condition quickly improves and the infiltrate resolves.

Infiltrative form of tuberculosis

This pathology has a blurred clinical picture; complaints may either be absent altogether or limited to:

• weakness;
• sweating;
• low temperature;
• cough with sputum, in which mycobacterium tuberculosis is detected during examination.

However, the radiograph reveals pronounced signs of infiltration of the lung tissue, often in combination with pleural effusion. Moreover, it is mainly the upper (sometimes middle) lobe of the lungs that is affected and antibiotic treatment is not effective.

Eosinophilic pulmonary infiltrate

With eosinophilic pulmonary infiltrate, a sharply increased number of eosinophils is detected in a blood test.

The disease is mild, physical symptoms are poor. Persons suffering from this pathology are concerned about weakness and an increase in body temperature to low-grade levels.

Eosinophilic infiltrates are detected not only in the lungs, but also in other organs (heart, kidneys, skin). An increase in eosinophils up to 80% is detected in the blood.

The reasons for this condition may be:

• helminthic infestation;
• taking antibiotics;
• introduction of radiopaque agents.

Pneumonia due to pulmonary infarction

Pulmonary infiltration in this disease is often preceded by pulmonary embolism. Such patients are concerned about:

• constant shortness of breath;
• chest pain;
• hemoptysis.

They usually have thrombophlebitis of the veins of the lower extremities.

Pneumonia due to obstruction of the bronchus by a tumor

This disease can manifest itself long before the infiltrative process is detected. It may be preceded by:

• prolonged low-grade fever;
• painful cough;
• hemoptysis.

Moreover, the infiltrate is usually determined in the upper or middle lobe of the lungs during X-ray examination, since the clinical picture is characterized by a paucity of objective signs. Examination of sputum reveals the presence of atypical cells in it.

Infiltration in pneumosclerosis

This pathological process is not an independent disease; it is the outcome of many chronic diseases of the lung tissue and consists in the replacement of pathological foci with connective tissue. Clinically, it does not manifest itself in any way. It can be determined on an x-ray or detected during an objective examination in the form of:

• areas of dullness upon percussion;
• weakened breathing upon auscultation.

Conclusion

Differential diagnosis of pulmonary tissue infiltration syndrome is extremely important, since the adequacy of the prescribed treatment and the outcome of the disease depend on the correct diagnosis. Moreover, patient management tactics and therapeutic measures can differ significantly and are determined by the disease, one of the manifestations of which is pulmonary infiltration.

Report by a specialist on the topic “Infiltration in the lung. Difficulties of differential diagnosis":

Source: otolaryngologist.ru

C-m respiratory failure

C-cavity formation in the lungs

C-m accumulation of air in the pleural cavity (pneumothorax)

S-th accumulation of fluid in the pleural cavity (hydrothorax)

S-m compaction of lung tissue

S-m pulmonary heart

With increased airiness of the lungs

C-m inflammatory obstruction of small bronchi

C-m inflammatory lesions of the tracheo-bronchial tree

S-m intoxication and nonspecific inflammatory changes

Intoxication syndrome (nonspecific)

Observed in all inflammatory diseases:

Increased body temperature

Weakness, malaise, weakness

Decreased appetite

Increased fatigue, sweating

Pain, aches in the body and muscles

Headache

Impaired consciousness (euphoria, agitation, delirium)

General inflammatory changes in the blood (leukocytosis, accelerated ESR, shift of the leukocyte formula to the left, positive CRP, increased fibrinogen content, increased alpha-2 and gamma globulins in the blood serum)

Lung compaction syndrome

1. Inflammatory infiltration of the lungs

2. Atelectasis of the lung

3. Local pneumofibrosis

4. Carnification of the lung

5. Tumor

This is both a nonspecific inflammatory process and specific inflammation (infiltrative pulmonary tuberculosis with edema) with exudation in the alveoli.

Typical objective data

Sometimes Sternberg's positive sm is on the losing side

Dullness or dullness to percussion

Harsh or bronchial breathing

Adverse respiratory sounds (moist rales, pleural friction noise, crepitus)

Atelectasis of the lung

AL is a violation of airiness as a result of collapse of the lung or part of it, due to the cessation of air access to the alveoli due to blockage or compression of the bronchus itself (enlarged lymph node, large amount of exudate in the pleural cavity)

Pathogenesis - when ventilation of areas of the lung ceases and while its blood supply is maintained, air is absorbed from the lung distal to the site of blockage, which causes collapse of the lung tissue or the lung is compressed from the outside.

A.L. - can be obstructive and compression

Obstructive atelectasis

Bronchial tumor

Foreign body

Compression of the bronchus from outside

Blockage of discharge (mucus, sputum)

Respiratory movements in this area of ​​the chest are limited.

With the duration of A.L. For more than 3 months, there is a retraction of part of the chest (due to a decrease in intrapulmonary pressure).

RG-uniform shading, with greater A. the median shadow (heart, large vessels) is shifted towards the lesion.

Compression atelectasis

Compression of the lung from outside (effusion into the pleural cavity, bleeding, etc.).

The area of ​​lung tissue above the fluid level is compressed and collapses, but bronchial patency is maintained.

In this case, a strip of lung tissue is determined above the fluid level, above which sound phenomena are heard characteristic of compaction of the lung tissue by the type of inflammatory infiltration (increased vocal tremor, dullness of percussion sound, harsh or bronchial breathing).

There are no adverse breath sounds.

Local fibrosis

It is detected in the lung tissue at the site of frequent repeated inflammation.

Objectively - manifested by all phenomena characteristic of tissue compaction, with the exception of adverse respiratory sounds

Carnification (a pathological process in which the pulmonary parenchyma changes its physical properties, acquiring the consistency and appearance of meat)

Most often, the outcome is pneumonia, when the inflammatory exudate (usually rich in fibrin) does not resolve, but is organized by sprouting connective tissue.

Objectively – manifested by all phenomena characteristic of compaction of lung tissue, with the exception of adverse respiratory sounds

Lung tumor

Peripheral cancer

Bronchial cancer (atelectasis often develops)

Objectively – all the signs characteristic of pulmonary tissue compaction syndrome (adverse respiratory sounds may also appear)

Pneumonia

Acute P. - acute exudative inflammatory processes of different etiology and pathogenesis, localized in the parenchyma and interstitial tissue of the lung, often involving the vascular system in the process.

Pulmonary parenchyma - respiratory bronchioles, alveolar ducts, alveolar sac, alveoli

Etiology of pneumonia

Infectious factor - bacteria, viruses, rickettsia, mycoplasma, chlamydia, legionella, fungi, etc.

Non-infectious factors

Chemical (petrol) – drivers

Physical (radiation)

Secondary infection

Pathogenesis of pneumonia

P. are divided into primary and secondary.

Primary - arise as independent diseases in a person with previously healthy lungs in the absence of diseases of other organs and systems.

Secondary – complicating other diseases (chronic bronchitis, congestive heart failure, postoperative, enzymatic (pancreatitis), autoimmune (collagenosis)

Microorganisms enter the lungs

Bronchogenic

Hematogenous

Lymphogenic

Airborne

Contagious (from nearby lesions - subhepatic abscess, mediastenitis)

Provoking factors

Smoking, Alcohol, Old age, Surgeries, Hypothermia, Viral infections

Classification of pneumonia -2

Moscow (1995) - 5th National Congress on Respiratory Diseases

Community-acquired

Intrahospital (hospital, nosocomial - more than 72 hours)

Atypical - caused by intracellular “atypical” pathogens (legionella, mycoplasma, chlamydia)

Pneumonia in patients with immunodeficiency conditions

Classification of pneumonia - 1

By etiology (bacterial, viral, due to physical and chemical factors, mixed

By pathogenesis (primary, secondary)

According to clinical and morphological characteristics (parenchymatous - lobar, focal, large-, small-focal, confluent, interstitial)

By location and length

Unilateral, bilateral (total, lobar, segmental, sublobar, central, basal)

By severity (mild, moderate, severe, extremely severe)

Along the course (acute, prolonged - more than 6 weeks)

Pathogens of pneumonia

1.Gr+ microorganisms:

Pneumococci (str. Pneumoniae) 70-96%, the most aggressive serotypes of pneumococci 1,2,3,6,7,14,19

Staphylococcus aureus (staph.aureus) 0.5-5%. With epidemic outbreaks up to 40%, a tendency to destruction

Pyogenic streptococcus (strep.pyogenes) 1-4%, during an influenza epidemic, complications of pleurisy, pericarditis are common

2.Gr- microorganisms:

Friedlander's bacillus (Klebsiella pneumoniae) 3-8%. Found in the oral cavity, sick after 40 years of age, severe course, viscous bloody sputum, confluent lesion, most often the upper lobe, foci of decay in the lung tissue, purulent complications

Escherichia coli (Escherichiae coli) 1-1.5%, for diabetes mellitus, confluent, in the lower sections).

Proteus (p. rettgeri, h. vulgaris, p. mirabilis, p. morgagni). In alcoholics, the upper lobe, decay.

Afanasyev-Pfeiffer bacillus (Hemophilus influenzae) 1-5%. Lives in the nasopharynx, during an influenza epidemic, with bronchitis, bronchiectasis, the lower lobe with involvement of the pleura

Pseudomonas aeruginosa (Pseudomonas aeruginosa) 3-8%. The causative agent of nosocomial infection, with concomitant glucocorticoid, cytostatic therapy

Legionella (Legionella pneumophille) 1.5%. Opening year 1976. Air-conditioned premises. Sometimes combined with diarrhea, high fever, acute renal failure.

3. Anaerobic pathogens (isolated cases, foul-smelling sputum)

4. Protozoa (Pneumocystis), HIV-infected patients, in weakened patients, after transplantation, with immunodeficiency, radiation therapy. The stages of the course are edematous, atelectatic, emphysematous stages. Romanovsky-Giemsa smears (pneumocystis)

5. Viruses (influenza, parainfluenza, respiratory syncytial, cytomegalovirus - during suppressive therapy, after transplantation)

6. Mycoplasma. More often in groups of people, discrepancy between severe intoxication, catarrhal symptoms and symptoms of lung damage

7. Chlamydia. Enlarged liver, lymph nodes, normal spleen, signs of pneumonia

8. Legionella.

Croupous (pleuropneumonia, lobar) pneumonia

KP is an acute inflammatory process of the pulmonary parenchyma involving a segment or lobe of the lung, which is based on a hyperergic inflammatory reaction, manifested by filling the alveoli with fibrin-rich exudate.

Etiology– pneumococci types 1-3.

Stages (path anatomy)

1st stage – high tide. Hyperemia of the lung tissue, inflammatory edema, 12 hours - 3 days.

Stage 2 – red liver, 1-3 days. The area of ​​inflammation is airless, dense, red in color with graininess on the cut.

Stage 3 – gray hepatization, 2-6 days. Neutrophils accumulate in the alveoli. The lung is gray-green in color.

Stage 4 – permits.

Clinic of lobar pneumonia

The onset is sudden, acute

Terrific chills

High fever, febris continua

Pleural pain on the affected side

Intoxication syndrome, “delirium tremens” - delirium tremens

Cough – dry at first, after 24 hours the sputum is “rusty”, scanty, viscous

Objectively – dullness, harsh or bronchial breathing, pleural friction noise, crepitao indux et redux

Lab. data – leukocytosis, shift to the left, accelerated ESR, toxic granularity of neutrophils, changes in the protein spectrum of the blood

Focal pneumonia (bronchopneumonia)

Acute AP is an acute inflammatory process of the pulmonary parenchyma involving a lobule or group of lobules.

Peculiarities pathogenesis acute AP

Volume of lesion (one or more lobules, segment, multiple foci)

Inflammation from the small bronchi spreads to the lung parenchyma (with lobar inflammation it spreads through the alveolar tissue through the Kohn pores)

An immediate hypersensitivity reaction in the respiratory area is not typical

Characteristic involvement of the bronchi in the inflammatory process

Impaired airway patency (possible microatelectasis)

The pleura is involved in the inflammatory process only when the inflammation is located superficially in the lungs

Morphological changes are not characterized by stages

The sputum is mucopurulent, serous (with CP there is a lot of fibrin)

Clinical features

Gradual onset of the disease (after ARVI)

Chest pain is rare (with a superficial location of the inflammation)

Cough from the very beginning with phlegm

Symptoms of intoxication are less pronounced

Shortness of breath is less common

Dullness of percussion sound is less pronounced

Breathing is often weakened vesicular

Wet fine rales (rarely pleural friction noise, crepitus is not observed)

The appearance of bronchophony is not typical

Syndrome of inflammatory changes of the tracheobronchial tree

Clinically presented by cough, sputum production. Hard breathing, dry wheezing.

Small bronchial obstruction syndrome

Reversible obstruction - inflammatory swelling of the bronchial mucosa - accumulation of viscous secretion, bronchospasm

Irreversible - narrowing of the bronchial lumen due to diffuse development of peribronchial sclerosis

Causes of bronchial obstruction – bronchitis, bronchospasm

Clinic of bronchial obstruction

Expiratory dyspnea

Extended exhalation

Dry wheezing on exhalation

Cough with difficult sputum

Development of emphysema

Bronchitis

Acute bronchitis– acute inflammation of the bronchial mucosa, characterized by an increase in bronchial secretion and clinically manifested by cough, and in some cases shortness of breath (with damage to the small bronchi)

Etiology

Infectious factors

Allergic factors

Chemical, physical factors (smoke, vapors of acids, alkalis, gases, etc.)

Pathogenesis– disturbance in the functioning of the mucociliary apparatus of the bronchi

Associated factors - unfavorable weather conditions (high humidity, cold air), smoking, alcoholism, decreased immunity, impaired mucociliary transport

Classification (by level of damage)

Tracheobronchitis (trachea and large bronchi)

Bronchitis (segmental bronchi)

Bronchiolitis (small bronchi, bronchioles)

Clinic

Cough, often paroxysmal, painful

First dry, then mucopurulent sputum

When the larynx is involved - barking

Slight rise in temperature

Objectively

Box shade of percussion sound

- breathing is harsh over the entire surface, dry wheezing (wet only when the smallest bronchi are involved)

Chronical bronchitis:

Diffuse, progressive damage to the bronchial tree, characterized by restructuring of the secretory apparatus of the mucous membrane, as well as sclerotic changes in the deeper layers of the bronchial walls and peribronchial tissue

CB - persons who have a cough with sputum for at least 3 months a year for 2 years in a row, excluding other diseases with such symptoms

The main criteria for chronic disease

Diffuse nature of the lesion of the bronchial tree both along the length and deep into the wall

Progressive course with periods of exacerbations and remissions

The dominant symptoms are cough, sputum, shortness of breath

Etiology

Infection

Atmospheric pollution (sulfur dioxide, pollutants, acid vapors, etc.)

Heredity (deficiency of ά1-antitrypsin, secretory Ig A)

Pathogenesis

Combination

Excess mucus production (hypercrinia)

Changes in the normal composition of the secretion (discrimination) and its viscosity

Mucociliary transport disorders

All these factors lead to the accumulation of secretions in the bronchial tree

Forms of chronic bronchitis

Chronic (simple) non-obstructive bronchitis– predominantly the proximal (large and medium) bronchi are affected, with a relatively favorable clinical course and prognosis. Clinical manifestations are a constant or intermittent cough with sputum production. Signs of bronchial obstruction only during periods of exacerbation and in the later stages.

Chronic obstructive bronchitis– along with the proximal and distal bronchi are affected. Clinically – cough, steadily increasing shortness of breath, decreased tolerance to physical activity.

Classification of chronic bronchitis

1.Form of CB – simple (non-obstructive), obstructive

2. Clinical, laboratory and morphological characteristics - catarrhal, mucopurulent, purulent

3. Phase of the disease - exacerbation, clinical remission

4. Severity – mild (FEV1-more than 70%), moderate (FEV1-from 50 to 69%), severe (FEV1-less than 50%)

5.Complications of chronic disease - pulmonary emphysema, DN (chronic, acute, acute on the background of chronic), bronchiectasis, secondary pulmonary hypertension, cor pulmonale (compensated, decompensated)

6.Primary CB and secondary CB (as a syndrome of other diseases, such as tuberculosis)

Chronic non-obstructive bronchitis

1. Damage to the bronchial mucosa by tobacco smoke, pollutants, repeated infections

2. Hyperplasia of goblet cells of the bronchial glands and hyperproduction of bronchial secretions (hypercrinia) and deterioration of the rheological properties of mucus (discrinia)

3. Violation of mucociliary clearance, protective and cleansing function of the bronchial mucosa

4. Focal degeneration and death of ciliated cells with the formation of “bald” spots

5. Colonization of damaged mucosa by microorganisms and initiation of a cascade of cellular and humoral inflammatory factors

6. Inflammatory edema and formation of areas of hypertrophy and atrophy of the mucosa

Clinic

1. Cough with mucous or mucopurulent sputum

2. Increased body temperature to subfebrile levels

3.Mild intoxication

4.Hard breathing

5.Dry scattered wheezing

6. At the height of exacerbation, symptoms of broncho-obstruction are possible due to the accumulation of viscous sputum in the bronchi and bronchospasm

7. In the remission phase, a cough with sputum is detected, there is no shortness of breath

Pathogenesis of chronic obstructive bronchitis

1. Inflammatory process in all bronchi (especially small ones)

2. Development of broncho-obstructive syndrome (combination of reversible and irreversible components)

3.Formation of pulmonary emphysema (centroacinar emphysema - due to early damage to the respiratory parts of the lungs - damage to the central part of the acinus)

4. Progressive impairment of pulmonary ventilation and gas exchange - leads to hypoxemia and hypercapnia

5. Formation of pulmonary arterial hypertension and chronic pulmonary heart disease

Clinic of chronic obstructive bronchitis

1. Expiratory shortness of breath, aggravated by physical activity and coughing

2. Boring, unproductive cough

3.Lengthening the expiratory phase

4.Secondary emphysema

5. Scattered dry wheezing (with quiet and forced breathing) and distant wheezing

Complications of chronic bronchitis

1.Infection related

Secondary pneumonia

Bronchiectasis

Infectious-allergic bronchial asthma

2. Associated with disease progression

Diffuse pneumofibrosis

Emphysema

Respiratory failure

Pulmonary heart

Chronic obstructive pulmonary disease

COPD is a disease characterized by irreversible bronchial obstruction, which has a progressive course and is associated with inflammation of the airways that occurs under the influence of unfavorable environmental factors (smoking, occupational hazards, pollutants). Its main symptoms are cough with sputum production and shortness of breath.

COPD is a heterogeneous group (COPD, emphysema, asthma, bronchiolitis obliterans, cystic fibrosis, bronchiectasis.

The unifying feature is inflammation of the mucous membrane of the respiratory tract, a violation of the ventilation function of the obstructive type.

Signs of exacerbation of COPD(Anthonisen et al.,1987 criteria)

1.Increase in sputum volume

2. Appearance of purulent contents in sputum

3. Appearance or progression of shortness of breath

Three types of exacerbations(important for assessing severity and treatment)

First - all three signs are present

Second - there are two signs

Third - there is one sign

Etiology and pathogenesis of COPD-1

Risk factors

Tobacco smoking (deterioration of mucociliary transport, decrease in the cleansing and protective function of the bronchi, promotes chronic inflammation of the mucous membrane, negative effect on surfactant - decrease in the elasticity of the lung tissue)

Occupational hazards (cadmium, silicon dust) – miners, builders, railway workers, workers associated with the processing of cotton, grain, paper

Respiratory viral infections

Hereditary predisposition

Etiology and pathogenesis of COPD-2

Risk factor – impact on the bronchial mucosa, interstitial tissue and alveoli – formation of a chronic inflammatory process – activation of neutrophils, macrophages, mast cells, platelets. Neutrophils – release of cytokines, prostaglandins, leukotrienes – formation of chronic inflammation.

The formation of pulmonary emphysema due to the destruction of the elastic framework of the lung tissue. The main cause of destruction is an imbalance in the “protease-antiprotease” and “oxidant-antioxidant” systems due to the pathogenic functioning of neutrophils.

A shift in the ratio of damage and repair processes, which are regulated by pro-inflammatory and anti-inflammatory mediators.

Impaired mucociliary clearance - colonization of mucous microflora - activation of neutrophils - increased destruction. Centroacinar and panacinar pulmonary emphysema is formed.

Emphysematous type of COPD

“Shortness of breath” - “pink puffing”. Symptoms of CB are less pronounced than the morphological and functional signs of emphysema. Asthenics and people of short stature predominate. Increased airiness due to the valve mechanism - “air trap”. Panacinar emphysema. At rest, there are no disturbances in the ventilation-perfusion relationship, and the normal gas composition of the blood is maintained. During physical activity there is shortness of breath and PaO2 decreases. Advanced DN, arterial hypertension and cor pulmonale develop late. Patients “puff”, puffing out their cheeks, there is no cyanosis for a long time, cor pulmonale – hence the name “pink puffers”.

Bronchitic type of COPD - “bluish edematous”

Centroacinar emphysema. Classic manifestations of COB. Hypersecretion of mucus, swelling of the mucous membrane, bronchospasm - increased resistance to inhalation and exhalation - arterial hypoxemia and shortness of breath, increased PaCO2, the occurrence of hypercapnia. Pulmonary hypertension and cor pulmonale develop earlier than in the emphysematous type. Dry wheezing, prolonged exhalation, cyanosis, peripheral edema are heard - the patient has “cyanotic edema”

Bronchial asthma

BA is a chronic relapsing disease, the obligatory pathogenetic mechanism of which is altered bronchial reactivity as a result of specific immunological (sensitization + allergy) or nonspecific mechanisms. The main clinical sign is an attack of suffocation due to bronchospasm and swelling of the bronchial mucosa.

Pathogenesis of asthma

Altered bronchial reactivity - disruption of narrowing/expansion processes, increased mucus production, disruption of its evacuation

Main pathogenetic variants BA

Exogenous (atopic, allergic)

Endogenous (non-atopic, non-allergic)

Aspirin BA

Autoimmune

Exercise asthma

Cholinergic variant of asthma

Night asthma

Cough variant of asthma

Professional BA

Dishormonal (hypoglucocorticoid deficiency, hyperestrogenism)

Neuropsychic (hysterical, neurasthenic, hypochondriacal)

Adrenergic imbalance (predominance of ά-adrenergic receptors over β-adrenergic receptors

Primary disorders of bronchial reactivity

BA Clinic

Attacks of suffocation of the expiratory type, which is based on bronchospasm + the appearance of viscous “vitreous” sputum

Three periods of suffocation

Precursors of suffocation (sneezing, dry nose, dry cough, vasomotor rhinitis, Quincke's edema)

The height of the attack (expiratory type suffocation, short inhalation and prolonged exhalation, wheezing, dry non-productive cough, forced position of the body with support on the hands, signs of DN (cyanosis, shortness of breath, changes in blood gases - PO2↓, PCO2), impaired venous outflow ( puffiness of the face), objective signs of bronchospasm

Reversal (cough with glassy sputum)

Complications of asthma

Pulmonary – status asthmaticus, emphysema, DN, pneumothorax

Extrapulmonary – cor pulmonale, heart failure

Asthmatic status - criteria

Progressive impairment of bronchial obstruction (severe asthma attack, worsening heart failure, diffuse cyanosis)

Rigidity to bronchodilators

Hypercapnia

Hypoxemia

Stages of status asthmaticus

Stage 1 – prolonged attack of asthma (dissonance between wheezing heard at a distance (there are many of them) and determined by a phonendoscope during auscultation (there are fewer of them)

Stage 2 – more severe condition of the patient, DN, “silent lung” – lack of breathing over a particular area or the entire lung

Stage 3 – development of a comatose state “red cyanosis” - hypercapnia, hypoxemia, acidosis

Mortality 20%

Emphysema

EL is a pathological expansion of air spaces distal to the terminal bronchioles, accompanied by destructive changes in the respiratory bronchioles and alveoli as a result of the pathogenic action of neutrophils accumulating in the intercellular space (definition of the American Lung Association)

Pulmonary heart syndrome

LS is a clinical syndrome caused by hypertrophy or dilatation of the right ventricle resulting from hypertension of the pulmonary circulation due to bronchial diseases, chest deformation or damage to the pulmonary vessels.

Acute drugs– 90% PE, pulmonary hypertension develops within a few hours

Subacute drugs– recurrent pulmonary embolism occurs over several weeks, months, repeated attacks of asthma

Chronic drug– occurs over several years

Pathogenesis of drugs

The basis of drugs is hypertension in the pulmonary circulation and the development of alveolar hypoxia. The Euler-Lillestrand reflex is important (increased tone of the pulmonary vessels in response to alveolar hypoxia), which leads to an increase in blood pressure in the pulmonary circulation - the pulmonary heart is formed

Clinic LS

Main lung disease + heart failure of the right ventricular type

Compensated LS = clinical picture of the underlying disease + right ventricular hypertrophy and/or right ventricular dilatation

Decompensated LS = clinical picture of the underlying disease + right ventricular hypertrophy and/or right ventricular dilatation + symptoms of cardiac right ventricular failure (swelling of the jugular veins, enlarged liver, edema, ascites)

Fluid in the pleural cavity

Pleural effusion is the accumulation of excess fluid in the pleural cavity, caused by inflammation of the pleura, impaired blood and lymph circulation, increased permeability of non-inflammatory capillaries, pleural tumors or other reasons.

1. Pleurisy (accumulation of exudate)

2.Hydrothorax (accumulation of transudate)

Cirrhosis of the liver

Hypoproteinemia in NS

Heart failure

3. Hemothorax (collection of blood)

4. Chylothorax (lymph accumulation)

Pleurisy

P – inflammation of the pleura, often with the formation of fibrinous plaque on its surface and effusion in the pleural cavity.

Pleurisy – dry (fibrinous) and effusion (exudative)

allergic (drug and other allergies, allergic alveolitis)

autoimmune (Dresler syndrome, rheumatism, rheumatoid arthritis, SLE, dermatomyositis, scleroderma)

post-traumatic (trauma, thermal, chemical, radiation damage)

Factors causing effusion

Increased secretion of inflammatory exudate into the pleural cavity

Microcirculation disorders, decreased resorption

Formation of fibrin film and connective tissue - decreased reabsorption of pleural fluid

Pleurisy clinic

Dry pleurisy (fibrinous)

Pneumonia

Pulmonary tuberculosis

Viral infection

Purulent-inflammatory processes in the lungs

1. Chest pain

2.Dry painful cough

3. Increased body temperature

4.Mussy's sign (sensitivity when pressing pressure points)

5.M.b. weakened vesicular breathing

6. Pleural friction noise (audible on inhalation and exhalation, increases with pressure with a stethoscope, does not change when coughing)

Exudative (exudative) pleurisy

Usually begins with fibrinous P.

Reduces chest pain

Signs of respiratory failure increase

Displacement of the mediastinum and trachea to the healthy side

Diffuse gray cyanosis

Expansion of the chest on the affected side, its lag in the act of breathing (Hoover's symptom), the intercostal spaces are smoothed (Litten's symptom), the skin fold on the affected side is more massive than on the healthy side (Wintrich's symptom)

Dullness (dullness) of percussion sound

The difference between exudate and transudate

Source: studopedia.ru

observed with lobar pneumonia, focal pneumonia, pulmonary tuberculosis and is characterized by an acute onset, high fever, chills, chest pain on the affected side, aggravated by deep breathing and coughing, as a result of which the patient is forced to suppress the cough, while breathing becomes shallow. From the 2nd day, a small amount of mucous, viscous sputum appears, sometimes containing streaks of blood. Quite quickly, the sputum acquires a brownish-red color (“rusty” sputum), which is caused by the breakdown products of red blood cells from the areas of the red liver. The amount of sputum secreted increases, but does not exceed 100 ml per day. In the stage of gray hepatization and especially resolution of the disease, the sputum becomes less viscous, easier to separate, and its brown color gradually disappears.
When examining a patient, already on the first day of the disease, flushing of the cheeks, more pronounced on the affected side, cyanosis of the lips, acrocyanosis may be noted, and herpetic rashes quite often appear on the lips, cheeks and wings of the nose. Quite often, when breathing, a wide movement of the wings of the nose is observed. Breathing, as a rule, is superficial, rapid, the affected side lags behind when breathing, the mobility of the pulmonary edge on the side of inflammation is limited.
When percussing the lungs, often already on the first day of the disease a shortening of the percussion sound over the affected lobe is detected, which, gradually increasing, takes on the character of a pronounced dullness (femoral tone). Vocal tremors at the beginning of the disease are somewhat intensified, and in the stage of hepatization they become clearly intensified.
Upon auscultation, at the beginning of the disease, breathing is weakened vesicular, and in the second stage it acquires a bronchial character. In the first days of the disease, in some cases, cripitatio indues is detected, and a small amount of scattered dry and moist rales can be heard. When the process spreads to the pleura, a pleural friction noise is heard.
In the second stage of the disease, symptoms of intoxication often appear: headache, irritability, lethargy, insomnia, severe weakness. In severe cases, agitation, confusion, delirium, symptoms of mental changes, and hallucinations may occur. Changes are also noted in other organs and systems: tachycardia, decreased blood pressure, sometimes even to the point of collapse, accentuation of the second tone over the pulmonary artery. Elderly and old people may develop signs of heart and coronary insufficiency, and sometimes heart rhythm disturbances.
An X-ray examination of the lungs reveals a homogeneous darkening of the corresponding lobe or segment. When examining blood: neutrophilic leukocytosis up to 20 - 109 l, shift to the left up to 6~30% of band neutrophils. Relative lymphopenia also occurs. Increased ESR, increased content of fibrinogen, sialic acids, seromucoid. Positive reaction to C-reactive protein. When examining urine during a febrile period, the following can be determined: moderate proteinuria, cylindruria, single red blood cells. In the resolution stage, well-being improves, cough decreases, percussion sound is muffled, breathing becomes harsh and then becomes vesicular, during this period crepitation (crepitacio redux), sonorous fine-bubble rales, the number of which gradually decreases, is heard.
NURSING DIAGNOSIS: fever, chills, chest pain, cough with mucopurulent or rusty sputum. Plan for examination, treatment and care of the patient.
IMPLEMENTATION OF THE PLAN: the nurse prepares the patient for an x-ray examination, collects biological material (blood, sputum) for laboratory testing, carries out medical appointments for the treatment of the patient (dispenses medications in a timely manner, makes various injections and infusions), prepares the patient for consultation with specialists (oncologist , phthisiatrician) according to indications, provides care for the patient (ventilation of the room, giving oxygen if necessary, timely change of underwear and bed linen, timely disinfection of spittoons, if necessary, feeding the patient, turning the patient in bed) and observation (monitors the respiratory rate, counts the pulse and heart rate, measures blood pressure, monitors physiological functions), places mustard plasters and cupping according to indications, etc.
ABSCESS SYNDROME IN THE LUNG is a severe process that occurs with severe intoxication, accompanied by necrosis and melting of the lung tissue with the formation of cavities. Lung abscess syndrome occurs in two stages: the infiltration or abscess stage and the cavity stage. The development of a suppurative process in the lung is associated with a violation of the drainage function of the bronchus, impaired blood supply and necrosis of the lung tissue, infection, and decreased reactivity
macroorganism. Abscess syndrome is characterized by constant or hectic fever, chills with profuse sweating, pain on the affected side, dry cough, but if accompanied by chronic bronchitis, there may be a small amount of mucous or mucopurulent sputum. Symptoms of intoxication are quite often observed: general weakness, malaise, loss of appetite, headache. An objective examination of the patient may reveal a lag in the affected half of the chest during breathing, weakened vocal tremor over the C1 abscess, weakened vesicular breathing, with concomitant K | In general bronchitis, dry buzzing wheezing may be heard, and upon percussion over the abscess there is a dull or dull percussion sound. X-ray examination reveals a rounded 4 shadow with clear edges. When examining blood: leukocytosis up to 20 ¦ 109 l, shift of the leukocyte formula to the left to metamyelocytes, increased ESR. A sharp increase in the amount of discharged purulent sputum (up to 500-1000 ml) with a fetid odor indicates a breakthrough of the abscess into the bronchus and its release. t
Blood streaks may be detected in the sputum. The condition of the patients improves, body temperature decreases, chills disappear and symptoms of intoxication decrease. You should pay attention to the fact that sputum is released more at a certain J position of the patient (drainage occurs). Physical examination reveals increased vocal tremors, tympanic, percussion sound, bronchial breathing, it can be amphoric, if the cavity is connected to the bronchus through a narrow gap. If a certain amount of secretion remains in the cavity, sonorous large- or medium-bubble rales may be heard. An X-ray examination reveals a rounded clearing with clear edges; if a secretion remains in the cavity, then an area of ​​darkening with a horizontal level is determined. When examining blood, leukocytosis and increased ESR remain, but with a tendency to decrease. When examining sputum, a significant number of leukocytes and elastic fibers are revealed.
NURSING DIAGNOSIS: fever, chills, chest pain, malaise, headache, cough with purulent sputum.
PLAN for examination, treatment, care and observation: preparing the patient for x-ray examination, for laboratory research, carrying out medical prescriptions for the treatment of the patient (timely distribution of medications, making injections and infusions), organizing other treatment methods (physiotherapy, exercise therapy, massage, oxygen therapy) , organization of care and monitoring of the patient.
IMPLEMENTATION OF THE PLAN: timely and targeted implementation of prescriptions (antibiotics of various spectrums, sulfonamides, nitrofurans, nystatin or levorin, mucolytics). Timely collection of biological material (blood, sputum, urine) for laboratory testing. Organizing a consultation with a physiotherapist to prescribe physiotherapeutic methods; exercise therapy doctor to prescribe exercise therapy and massage. Organization of timely ventilation of the room, wet cleaning with disinfectants, washing and disinfection of the spittoon, timely change of underwear and bed linen, prevention of bedsores, regular turning of the patient to create drainage and discharge of sputum - 4-5 times a day for 20-30 minutes; monitoring the activity of the cardiovascular system (pulse, heart rate, blood pressure measurement), bronchopulmonary system (respiratory rate, amount of sputum produced), physiological functions.
PLEURAL FLUID SYNDROME
CAVITIES (exudative pleurisy) - is an inflammatory lesion of the pleura, accompanied by the accumulation of fluid in the pleural cavity. The development of the inflammatory process in the pleura is facilitated by exacerbation of the tuberculosis process in the lungs and intrathoracic lymph nodes (tuberculosis intoxication), chronic nonspecific lung diseases (pneumonia, suppurative processes in the lungs), acute and chronic infectious diseases (typhoid and typhus), rheumatism, collagenosis, tumors lungs. The provoking factor is usually hypothermia. This syndrome is characterized by inflammation of the pleural layers and, first of all, the deposition of fibrin on them. According to the nature of the fluid in the pleural cavity, pleurisy can be serous-fibrinous, hemorrhagic, purulent, chylous and mixed. If there is fluid in the pleural cavity of non-inflammatory or unknown origin, they speak of pleural effusion.
The disease begins gradually or acutely, with high fever, severe stabbing pain in the chest, aggravated by taking a deep breath or bending to the healthy side and coughing. The cough is usually dry and painful. The examination reveals a forced position of the patient on the affected side, shortness of breath, cyanosis, and lag of the affected side of the chest when breathing. When fluid accumulates, patients feel a feeling of heaviness and dull pain on the affected side; if a lot of fluid accumulates, then a shift of the mediastinum to the healthy side may occur and severe shortness of breath appears. The fluid, as a rule, is located along a parabolic curve (Damoiso line), its apex is located along the posterior axillary line. In this regard, three zones are distinguished: the prestressed zone

lung to the root (Garland's triangle), a zone of hydrothorax and a zone of displaced mediastinum to the healthy side (Rauchfuss-Grocco triangle). With physical methods of examination in the area of ​​​​a compressed lung (compression atelectasis), palpation is determined by increased vocal tremors and bronchophony, a tympanic percussion sound, and auscultatory bronchial breathing. In the hydrothorax zone: vocal tremor and bronchophony, as well as breathing, are not detected; the femoral tone is determined by percussion. The same is determined in the zone of mediastinal displacement (Rauchfus-Grocco triangle).
After the examination (obtaining information about the patient), a NURSING DIAGNOSIS is made: fever, chest pain, shortness of breath, dry cough, weakness, malaise. A PLAN is being drawn up for monitoring and caring for the patient, laboratory and instrumental research methods, carrying out medical treatment prescriptions and consulting a phthisiatrician and oncologist. When implementing the IMPLEMENTATION OF THE PLAN, great importance is given to preparing the patient for an x-ray examination, collecting biological material for laboratory testing, preparing the patient for pleural paracentesis, and strictly following medical prescriptions in the treatment of the patient: timely distribution of medications and injections. An X-ray examination reveals darkening on the affected side with an oblique fluid level.
Pleural puncture (pleural paracentesis) has important diagnostic and therapeutic significance. The nurse should prepare for this purpose a sterile syringe for anesthesia, a solution of novocaine, a solution of iodine and alcohol for treating the skin, a puncture needle with a rubber tube with cannulas for the needle and syringe, a Mohr or Pean clamp, a 50 ml Janet syringe, and a container for collecting pleural fluid. punctate. Paracentesis is performed in the 8th intercostal space along the upper edge of the 9th rib along the posterior axillary line. After receiving the punctate, the content of bek in it, the density of the pleural fluid are determined and the Rivalta test is performed to identify exudate or transudate. The basic principles of treatment are to prescribe anti-inflammatory and anti-tuberculosis drugs, restoratives, vitamin therapy; after evacuation of pleural fluid, exercise therapy and physiotherapeutic procedures are prescribed after consultation with a physiotherapist to prevent adhesions.
CHOKING SYNDROME. Most often, this syndrome is caused by a disease such as bronchial asthma. By bronchial asthma we mean allergosis with a predominant localization of hyperergic inflammation in the bronchopulmonary apparatus, 24

characterized by recurrent, predominantly generalized, airway obstruction, reversible in the early stages of the disease. There are atopic (non-infectious-allergic) and infectious-allergic bronchial asthma. In atopic asthma, the cause can be any substance that can cause the formation of antibodies in the human body. Allergens can be of animal and plant origin, as well as chemical substances with simple and complex structures.
In the infectious-allergic form, the cause of the development of bronchial asthma is microbial flora. In addition, the etiological factors for the development of bronchial asthma are psychogenic, climatic (hypothermia, insolation) factors, as well as severe physical activity. Moreover, these factors, as a rule, are provocative and can sometimes be triggers for the development of asthma. Clinical manifestations: the leading clinical symptom complex of bronchial asthma is expiratory shortness of breath, wheezing, periodic attacks of suffocation (generalized obstruction), often ending in the discharge of a significant amount of sputum. The atopic form of bronchial asthma is characterized by the sporadic development of an attack of suffocation upon contact with an allergen. The cessation of exposure to the allergen causes the cessation of the attack. In this case, suffocation is usually preceded by an aura, characterized by a pronounced polymorphism of manifestations (vasomotor rhinitis with copious discharge of watery secretions, migraine, urticaria, itching, soreness and soreness in the throat, cough, Quincke's edema, etc.). Attacks of suffocation in infectious-allergic bronchial asthma develop against the background of acute respiratory diseases, bronchitis and pneumonia, more often in the autumn-winter period. The aura in patients of this group in most cases is expressed by coughing. The attacks are usually moderate or severe, quite long-lasting and resistant to conventional therapy, and often transform into an asthmatic state. The most common sensitivity is to staphylococcal toxin and streptococcus. The main clinical symptoms of an attack of suffocation are expiratory shortness of breath due to limited mobility of the chest (low position of the diaphragm), wheezing, scattered dry whistling and buzzing rales, constantly changing their intensity and location. The patient always assumes a forced orthopneic position with fixation of the shoulder girdle: the patient sits, leaning his hands on the edge of the table, bending forward. The skin is pale, the auxiliary muscles are tense, the cardiovascular system has tachycardia, dullness of heart sounds, the boundaries of absolute cardiac dullness are not determined due to pulmonary emphysema.
In the case of an infectious-allergic form of asthma, the attack ends with the discharge of a significant amount of viscous mucopurulent sputum. If the attack is prolonged, then a pronounced depressive state of the patient is noted, pallor of the skin is replaced by warm cyanosis of the skin of the face and limbs, and as a result of developing tissue hypoxia in the heart, anginal pain may occur. During a severe attack of suffocation, fractures of those ribs to which the anterior scalene and external oblique muscles are attached may be observed. Their opposite action during coughing can cause a rib fracture. The formation of spontaneous pneumothorax, interstitial or mediastinal emphysema is possible. A fairly serious complication is the occurrence of acute emphysema, as well as a large emphysematous cyst (bulla). During physical examination, the following is noted: palpation resistance of the chest, weakening of voice tremors; percussion - box tone, significant limitation of mobility of the pulmonary edge and drooping of the lower border of the lungs; Auscultation - weakened vesicular breathing, a lot of dry whistling, less often buzzing wheezing.
NURSING DIAGNOSIS: suffocation with prolonged exhalation, cough, mostly dry, tachycardia, cyanosis.
PLAN for monitoring and caring for the patient, preparing the patient for additional research methods, collecting biological material (blood, sputum) for laboratory testing, carrying out medical prescriptions for treating the patient, providing pre-medical emergency care, preparing the patient for consultation with other specialists.
IMPLEMENTATION OF THE PLAN OF THE ACTIVITY OF THE NURSE. First of all, the nurse should provide first aid in case of an attack of suffocation: calm the patient, create physical and mental peace, create a comfortable position for the patient, open a window (window, transom) for access to fresh air, give oxygen, put mustard plasters, give a warm drink, report to the attending or duty doctor and then follow the doctor’s orders. When examining peripheral blood at the height of an attack, eosinophilia and basophilia are revealed. When examining sputum, a triad is characteristic: an increased content of eosinophils, the presence of Charcot-Leyden crystals and Kurshman spirals. When studying the function of external respiration in patients at the height of an attack of suffocation, a decrease in vital capacity is detected, the residual volume and functional residual capacity increase significantly. An important feature is pronounced disturbances of bronchial obstruction.
PRINCIPLES OF TREATMENT: etiological therapy for the atopic form of bronchial asthma is possible when the allergen is identified. It is necessary to eliminate the allergen from the patient’s everyday life, follow a diet that excludes allergenic foods, and take hygienic measures if patients are sensitive to house dust. If it is impossible to eliminate the allergenic factor, specific or nonspecific desensitizing therapy is necessary. Contraindications to desensitizing therapy are the presence of pulmonary tuberculosis, pregnancy, decompensated cardiosclerosis, decompensated rheumatic heart disease, thyrotoxicosis, decompensated kidney disease, liver disease, mental illness, severe pulmonary insufficiency.
ACUTE bronchial inflammation syndrome, or acute bronchitis, is a fairly common respiratory disease. Most often, acute inflammation of the bronchi is observed in patients with acute respiratory diseases caused by influenza, parainfluenza, adenoviral infection, as well as in severe forms of measles, whooping cough, and diphtheria. Acute bronchitis caused by bacterial agents against the background of exposure to the influenza virus, which inhibits phagocytosis and leads to activation of the bacterial flora of the respiratory tract, is quite common. In the sputum of such patients, influenza bacillus, pneumococci, hemolytic streptococcus, Staphylococcus aureus, Friedlander's bacillus, etc. are found. Predisposing factors may be hypothermia, alcohol abuse, chronic intoxication, smoking, in addition, the presence of foci of infection in the upper respiratory tract (tonsillitis, rhinitis, sinusitis, etc.) also contributes to the occurrence of acute bronchitis. Other causes of acute bronchitis include inhalation of air containing high concentrations of nitrogen oxides, sulfuric and sulfur dioxide, hydrogen sulfide, chlorine, ammonia, bromine vapor, as well as exposure to chemical warfare agents (chlorine, phosgene, diphosgene, mustard gas, lewisite, FOB ). A fairly common cause of acute bronchitis can be inhalation of air with a high content of dust, especially organic dust.
CLINICAL MANIFESTATIONS: the appearance of a dry, irritating cough, a feeling of rawness or pain in the chest, then the process moves to large and small bronchi, which leads to symptoms of airway obstruction (paroxysmal cough, shortness of breath). On days 2-3, mucous or mucopurulent sputum begins to separate, sometimes mixed with blood. Most patients experience pain in the lower parts of the chest caused by coughing and convulsive contraction of the diaphragm, general weakness, malaise, weakness, pain in the back and limbs, and often sweating. Body temperature can be normal or subfebrile, and in severe cases it rises to 38°C. If acute bronchitis is of influenza etiology, then the temperature often rises to 39°C and higher, and heipes labialis, hyperemia of the mucous membranes of the pharynx and pharynx, often with pinpoint hemorrhages, is often detected.
On percussion there is a pulmonary sound. Auscultation in the first days of the disease reveals vesicular breathing with prolonged exhalation, scattered dry whistling and buzzing wheezing, and when coughing, the amount of wheezing changes. After 2-3 days, moist rales of various sizes usually appear. From the cardiovascular system - tachycardia, from the nervous system - headache, weakness, poor sleep.
NURSING DIAGNOSIS: cough, malaise, weakness, shortness of breath, tachycardia, fever, poor sleep.
DEVELOPING A PLAN for nursing interventions: care and observation, examination and implementation of medical prescriptions for the treatment of patients.
IMPLEMENTATION OF THE PLAN OF NURSING ACTIVITIES: independent - methods of care and monitoring of the patient: pulse rate, respiration, heart rate, blood pressure measurement, physiological functions, general condition, room ventilation, placement of mustard plasters, cupping;
dependent - collection of biological material (blood, urine, sputum) for laboratory testing, preparing the patient for an X-ray examination of the chest, examination of external respiration function, timely distribution of medications, administration of medications parenterally. A blood test reveals leukocytosis of 8-109 l, accelerated ESR; there is a significant amount of microflora in the sputum; when examining the function of external respiration, a decrease in vital capacity and maximum ventilation is revealed; when small bronchi are involved in the process, a violation of bronchial patency and forced vital capacity is detected; X-ray examination sometimes reveals an expansion of the shadow at the root of the lungs. A consultation with a physiotherapist is organized to prescribe physiotherapeutic treatment (electrophoresis with potassium iodide, calcium chloride, euphilin, etc., exercise therapy).
PRINCIPLES OF TREATMENT: Treatment is often carried out at home, where the patient should avoid sudden changes in ambient temperature. From medications - anti-inflammatory media

agents: amidopyrine, analgin, aspirin, which have antipyretic and analgesic effects.
In case of severe acute bronchitis during an influenza epidemic, in elderly and elderly people, as well as weakened patients, hospitalization and the prescription of tablet antibiotics and sulfonamides in general doses are advisable.
To liquefy sputum, infusions of thermopsis, ipecac, infusions and extracts of marshmallow root, mucaltin, 3% solution of potassium iodide, alkaline inhalations, and exercise therapy are prescribed. In the presence of bronchospasm, bronchodilators are prescribed: tablets of theophedrine, ephedrine 0.025 g and euphilin 0.15 g 3 times a day.
For a dry, painful cough, you can prescribe: codeine, dionine, hydrocodone, libexin, baltika. Distractions are prescribed: mustard plasters on the chest and back, cupping, warm foot baths, plenty of warm drinks, and alkaline mineral waters.
To prevent the transition of acute bronchitis to chronic, complex therapy should be continued until the patient recovers completely.
CHRONIC bronchial inflammation syndrome is
chronic bronchitis, which is a diffuse inflammation of the mucous membrane of the bronchial tree and the deeper layers of the bronchial wall, characterized by a long course with periodic exacerbations. According to WHO experts, “patients with chronic bronchitis include those who have a cough with sputum for at least three months a year for two years, excluding other diseases of the upper respiratory tract, bronchi and lungs that could cause these symptoms.” This is a fairly common disease of the bronchopulmonary system; it should be noted that the incidence is increasing. People over 50 years of age are more likely to get sick, and men get sick 2-3 times more often.
Factors contributing to the occurrence of chronic bronchitis should be considered, first of all, constant irritation of the mucous membranes of the respiratory tract by polluted air. Unfavorable climatic conditions are also important: a damp climate with frequent fogs and sudden changes in weather. Irritation of the mucous membranes of the respiratory tract by dust or smoke, especially tobacco, is a trigger for increased mucus production in the respiratory tract, which leads to coughing and sputum production, and easier infection of the bronchial tree. Chronic bronchitis occurs 3-4 times more often among smokers than among non-smokers. Big
importance in the etiology of chronic bronchitis is given to exposure to occupational hazards - among workers in wool and tobacco factories, flour mills and chemical plants, miners, miners. Pollution of large cities with sulfur dioxide, acid vapors, vehicle exhaust gases, and smoke particles is also of no small importance.
The development of chronic bronchitis is facilitated by long-existing foci of infection in the respiratory tract (chronic tonsillitis, sinusitis, bronchiectasis), congestion in the pulmonary circulation (with heart failure). The addition of an infection worsens the course of chronic bronchitis, leads to the spread of the inflammatory process to the deeper layers of the bronchial wall, damage to its muscle and elastic fibers. In the etiology of chronic bronchitis, especially in the development of its exacerbations, the participation of a bacterial infection has been established. Most often, staphylococci, streptococci, influenza bacillus and pneumococci are cultured from sputum or bronchial contents, and less commonly, Pseudomonas aeruginosa and Friedlander's bacillus. The frequency of exacerbations of chronic bronchitis increases sharply during periods of influenza epidemics. Currently, certain importance is attached to factors of hereditary predisposition to the development of chronic processes in the bronchopulmonary system.
CLINICAL MANIFESTATIONS: the most common and main symptoms of chronic bronchitis are cough (dry or wet), sputum production of varying amounts and nature, impaired pulmonary ventilation and bronchial obstruction. Most patients, usually smokers, have had a slight cough for several years, dry or with mucous sputum, mainly in the morning, which patients do not attach importance to. Gradually, the cough becomes more pronounced, causes inconvenience, intensifies in cold and damp weather, after hypothermia, upper respiratory tract infections and is accompanied by periodic separation of mucopurulent or purulent sputum. In the initial period of the disease, large bronchi are affected. The disturbance of bronchial obstruction is insignificantly expressed, the development of shortness of breath occurs slowly, exacerbations are characteristic, accompanied by a cough with the release of a large amount of purulent or mucopurulent sputum. As the disease progresses and the small bronchi are involved in the process, bronchial obstruction occurs (obstructive bronchitis) with the development of shortness of breath. At first, shortness of breath bothers you during physical activity, then it becomes constant. Its severity increases during periods of exacerbation. In patients with predominant damage to the small bronchi, in addition to shortness of breath, cyanosis and paroxysmal cough are observed, which intensifies when moving from a warm room to a cold one. The natural course of obstructive bronchitis is the development of emphysema and chronic pulmonary heart disease.
At any stage of the disease, the addition of bronchospastic syndrome, characterized by the development of expiratory dyspnea, can be observed. Cases where bronchospasm is the leading clinical picture of the disease and at the same time there are signs of allergy (vasomotor rhinitis, drug or food allergies, eosinophilia in the blood, the presence of eosinophils in the sputum) are usually referred to as asthmatic bronchitis. During periods of exacerbation of the disease, an increase in body temperature, often up to low-grade levels, general weakness, sweating, increased fatigue, pain in various muscle groups associated with overstrain when coughing are observed.
The percussion sound at the beginning of the disease is little changed, but with the development of emphysema, a box sound and a decrease in the mobility of the lower edges of the lungs are determined.
During auscultation during the period of remission of the disease, breathing can be vesicular, or in the presence of emphysema, weakened vesicular breathing can be heard. In some areas, breathing may be harsh, with a small amount of wheezing. During an exacerbation, dry or moist rales are heard, the number of which can vary widely. In the presence of bronchospasm against the background of an extended outlet, dry wheezing rales are heard, the number of which increases with forced breathing.
NURSING DIAGNOSIS: dry or wet cough, shortness of breath, malaise, fatigue, sweating, fever.
PLAN of examination, care and observation, principles of treatment.
IMPLEMENTATION OF THE PLAN: independent - methods of care and monitoring of the patient are used; dependent - collecting biological material (blood, urine, sputum) for laboratory testing, preparing patients for x-ray examination, bronchoscopy, timely distribution of medications, making injections and infusions as prescribed by the doctor. A blood test reveals moderate neutrophilic leukocytosis and accelerated ESR. In patients with asthmatic bronchitis - eosinophilia. In the presence of emphysema and respiratory failure, erythrocytosis is observed with a slight increase in hemoglobin levels. From biochemical studies, an increase in the content of fibrinogen, sialic acids, and C-reactive protein may be observed
When examining sputum in patients with asthmatic bronchitis, eosinophils, Charcot-Leyden crystals, and Courshman spirals may be detected. An X-ray examination reveals a heavy pulmonary pattern; in the presence of emphysema, an increase in the transparency of the pulmonary fields, low standing and flattening of the diaphragm, and a decrease in its mobility. Bronchoscopy may reveal narrowing or torsion of the bronchi, a decrease in the number of lateral bronchial branches, and cylindrical and saccular bronchiectasis.
PRINCIPLES OF TREATMENT: in case of exacerbation of the disease, it is advisable to carry out treatment in a hospital. Treatment must be comprehensive. The main component during periods of exacerbation is antibacterial therapy. The effectiveness of antibiotic therapy increases if it is carried out taking into account the sensitivity of the isolated microflora to antibiotics. Treatment of exacerbations in patients with long-term chronic bronchitis requires the use of broad-spectrum antibiotics. Sulfonamides are used less frequently. For the prevention and treatment of fungal complications, nystatin and levorin are used. To restore the drainage function, expectorants are used (thermopsis infusion, marshmallow root in the form of infusions and extracts); a very effective expectorant is a 3% solution of potassium iodide; in the presence of viscous sputum, enzymes (trypsin, chemotrypsin, chymopsin, ribonuclease, etc.) are used in the form of aerosol inhalation. Codeine should be used only for dry, hacking, debilitating cough. Better discharge of sputum is facilitated by inhalation of alkaline solutions, drinking plenty of hot drinks, and taking alkaline mineral waters. For bronchospasm, the following are prescribed: ephedrine, novodrine, etc. One of the components of complex therapy are desensitizing and antihistamine drugs (diphenhydramine, suprastin, pipolfen, calcium gluconate, aspirin, etc.). For persistent bronchospasm, corticosteroid therapy is indicated. In severe exacerbations, an important place belongs to therapeutic bronchoscopy, during which the bronchi are washed with Ringer's solution, furagin or soda, removing purulent contents, casts of the bronchi, plugs and introducing drugs (antibiotics, hormones, enzymes) into the bronchial tree; when the process subsides, physiotherapeutic procedures (sollux, ultraviolet irradiation, UHF currents, electrophoresis with novocaine, calcium chloride on the chest, exercise therapy).
SYNDROME OF INCREASED AIR TISSUE OF PULMONARY TISSUE (pulmonary emphysema). The term “pulmonary emphysema” (from the Greek emphysae - to blow, to inflate) refers to pathological processes in the lungs, characterized by an increased content of air in the lung tissue.

There are primary and secondary emphysema. The most common form is secondary diffuse emphysema, which develops as a result of chronic obstructive pulmonary diseases (acute and chronic bronchitis, bronchial asthma, etc.).
In the development of pulmonary emphysema, factors that increase intrabronchial and alveolar pressure with the development of swelling of the lungs (prolonged cough, overstrain of the external respiratory apparatus in glassblowers, musicians playing wind instruments, singers, etc.), changes in the elasticity of the lung tissue and mobility of the chest with age (senile emphysema).
In the development of primary emphysema, hereditary factors play a role, in particular, hereditary deficiency of α1-antitrypsin. With a deficiency of the latter, there is a decrease in the protection of the mucous membranes of the bronchial tree and pulmonary parenchyma from the damaging effects of proteolytic enzymes released from leukocytes and microbial cells during repeated episodes of inflammation. These “excess enzymes” can lead to damage to elastic fibers, thinning and rupture of the alveolar septa.
Emphysema can be interstitial or alveolar. Interstitial emphysema is characterized by the penetration of air into the lung stroma (peribronchial, perilobular), and is often combined with mediastinal emphysema and subcutaneous emphysema. Alveolar emphysema is more common due to increased air content in the alveoli. Alveolar emphysema can be diffuse or localized.
The most common form - alveolar diffuse emphysema - is a consequence of chronic obstructive pulmonary diseases. In the presence of obstruction during exhalation, breathing becomes difficult and occurs mainly due to the additional work of the respiratory muscles. Disturbances in ventilation processes develop during each respiratory act, a decrease in intra-alveolar oxygen tension and an increase in carbon dioxide tension occur. Violation of intra-alveolar ventilation causes increased stretching of the alveoli and contributes to the loss of elasticity of the interalveolar septa. Stretching the walls of the alveoli leads to difficulty in blood flow in the adjacent

Infiltration – excessive penetration and accumulation of effusion in the alveoli, containing various cellular elements, chemicals (biologically active substances).

Depending on the cause and nature of the effusion, infiltration occurs:

- inflammatory(for pneumonia, tuberculosis, fibrosing alveolitis, diffuse connective tissue diseases);

- non-inflammatory(for lung cancer, leukemia, pulmonary infarction).

Clinical manifestations:

· cough;

shortness of breath;

· pain in the chest - only when the pleura is involved in the pathological process;

· hemoptysis – with destruction of lung tissue, tuberculosis, staphylococcal pneumonia, lung cancer.

General inspection:

“warm cyanosis” caused by respiratory failure;

· forced position on the sore side when the pleura is damaged.

General examination of the chest:

· static – asymmetrical bulge on the affected side in children;

· dynamic – lag of the affected half in the act of breathing, tachypnea.

Palpation of the chest:

· in the initial and final stages of infiltration - tympanic sound;

· at the height of infiltration – dull or dull sound.

Topographic percussion: decreased mobility of the lower pulmonary edge on the affected side.

Auscultation of the lungs:

In the initial stage of infiltration:

The appearance of silent crepitation (crepitatio indux).

In progress:

Vesicular breathing and crepitus disappear, bronchial breathing appears.

In the stage of resolution (resorption) of the infiltrate:

Weakening of vesicular breathing;

Sound crepitation (crepitatio redux) + sonorous moist fine rales;

There may be wheezing, pleural friction noise;

Bronchophony is enhanced.

Instrumental diagnostics:

· the main method of examination is radiography of the lungs in frontal and lateral projections - the presence of shadows;

· spirography is a restrictive type of dysfunction of external respiration caused by respiratory failure or mixed with broncho-obstructive syndrome.

Clinical symptoms of intoxication syndrome:

Complaints:

general complaints:

Fever;

General weakness, malaise;

Sweating;

Myalgia;

Cardiac complaints - palpitations, fainting, asthma attacks;

· cerebral complaints – headaches, sleep disturbances, delirium, hallucinations, confusion;

· dyspeptic complaints – loss of appetite, nausea, vomiting.

Peculiarity: pneumonia caused by mycoplasma, chlamydia, legionella occurs with a predominance of general intoxication syndrome, bronchopulmonary manifestations are scanty, therefore these pneumonias are called “atypical”.

Changes detected during general examination patients with pneumonia:

· consciousness – depressed to the point of hypoxic coma with extremely severe pneumonia, acute respiratory failure;

Delusions, hallucinations in children, alcoholics due to intoxication;

· there may be a forced position on the sore side;

· cold skin, cyanosis with a marble tint;

· herpetic rashes on the lips and wings of the nose;

· feverish face, blush on the affected side.

Respiratory examination– manifestations of pulmonary tissue infiltration syndrome.

– tachycardia, accent of the second tone on the pulmonary artery, hypotension.

Laboratory diagnosis of pneumonia:

· general blood test: leukocytosis, shift of the formula to the left, toxigenic granularity of neutrophils, increased ESR - inflammatory changes;

for viral pneumonia: leukopenia, relative lymphocytosis.

· biochemical blood test – increased fibrinogen levels, positive C-reactive protein – acute phase indicators; in severe cases - laboratory manifestations of renal and liver failure;

· immunological blood test - for viral, atypical pneumonia - detection of diagnostic titer of specific antibodies;

· sputum analysis: - general (microscopic): many leukocytes, macrophages, bacterial flora - Gram staining, detection of atypical cells, BK - differential. diagnostics;

Bacteriological: pathogen verification, identification

its sensitivity to antibiotics; significant amount

10 5 – 10 7 microbial bodies in 1 ml.

· General urine analysis - there may be febrile proteinuria, hematuria.

Instrumental diagnosis of pneumonia:

· R-graphy of the chest organs in 2 projections – the main method is focal and infiltrative opacities, enhancement of the pulmonary pattern;

· R-tomography, computed tomography of the lungs - for abscess formation - for differential diagnosis with tuberculosis, lung cancer.

· Bronchoscopy – for suspected cancer, foreign body, therapeutic – for abscess formation.

· ECG – in severe cases to identify signs of overload of the right side of the heart.

· Spirography – in the presence of other diseases of the respiratory system.

Basic principles of treating pneumonia:

· gentle mode;

· good nutrition;

· drug therapy:

Etiotropic: antibacterial, antiviral, fungal, antiprotozoal;

Detoxification - saline solutions;

Pathogenetic – for severe and complicated pneumonia:

anticoagulants (heparin), antienzyme drugs (contrical), glucocorticoids, oxygen therapy, antioxidant therapy, immunocorrective therapy;

Symptomatic therapy: bronchodilators, mucolytics, analgesics, antipyretics;

Non-drug treatment:

Physiotherapeutic treatment – ​​UHF, magnetic therapy, laser therapy, EHF therapy;

Exercise therapy, breathing exercises.

Pleurisy is an inflammation of the pleura with the formation of effusion on its surface or accumulation in its cavity.

This is not an independent disease, but a manifestation or complication of many diseases.

Etiopathogenetic classification of pleural lesions:

1. Inflammatory (pleurisy):

a) infectious

b) non-infectious:

allergic and autoimmune:

for rheumatic diseases:

· enzymatic: pancreatogenic;

· traumatic, radiation therapy, burns;

· uremic.

2. Non-inflammatory:

· tumor lesions of the pleura;

· congestive – with left ventricular heart failure;

dysproteinemic pleural effusions;

· other forms of effusion accumulation - hemothorax, chylothorax;

· presence of air in the pleural cavity – pneumothorax.

By criterion for the presence of effusion pleurisy occurs:

Dry (fibrinous);

Exudative.

By character effusion exudative pleurisy occurs:

Serous;

Serous-fibrinous or hemorrhagic;

Purulent (pleural empyema).

By flow pleurisy is:

Subacute;

Chronic.

Pathogenesis:

1. increased permeability of the vessels of the parietal pleura with excessive sweating of fluid, proteins and blood cells into the pleural cavity;

2. disturbance of resorption of pleural fluid by the diaphragmatic part of the parietal pleura and lymph flow;

3. a combination of the first 2 factors most often.

With moderate exudation into the pleural cavity with preserved outflow, fibrinous pleurisy is formed due to the loss of fibrin from the exudate onto the surface of the pleura. With severe exudation and impaired resorption - exudative pleurisy. When the exudate is infected with pyogenic flora - pleural empyema.

Clinical manifestations of fibrinous (dry) pleurisy syndrome:

Complaints: 1) acute pain in the chest, aggravated by taking a deep breath, coughing, or bending to the healthy side;

2) non-productive cough.

During general examination a forced position on the sore side is revealed.

Chest examination– tachy-, hypopnea, lag of the affected half of the chest in the act of breathing, decreased excursion of the chest.

Palpation of the chest: pain when pressing in the area of ​​pleural overlays. A pleural friction rub may be detected.

Percussion – limited mobility of the lower edge of the lungs on the affected side is determined.

Auscultatory a sign of fibrinous pleurisy is a pleural friction noise.

Clinical manifestations of exudative pleurisy:

Complaints 1) a feeling of heaviness, fullness in the affected half of the chest;

2) inspiratory dyspnea;

3) non-productive cough;

4) fever, chills, sweating.

During general examination a forced position on the sore side is revealed; for massive effusion - sitting; "warm" cyanosis.

Chest examination:

Enlargement of the affected half of the chest;

Expansion and bulging of intercostal

gaps;

Lagging of the affected half of the chest in the act of breathing.

Percussion a dull sound with an oblique upper border is detected (Damoizo-Sokolov line).

Auscultation of the lungs. In the area of ​​accumulation of effusion, breathing is not detected; pleural friction noise can be heard above its upper border; in the area of ​​Garland’s triangle, bronchial breathing can be heard. There is no bronchophony over the effusion.

Cardiovascular examination: swelling of the neck veins, rapid pulse, tachycardia. The apical impulse and the boundaries of relative dullness of the heart are shifted to the “healthy” side. On the affected side, manifestations of lung collapse can be detected.

Clinical manifestations of pleural empyema the same as for exudative pleurisy. The peculiarity of the expression of intoxication is febrile hectic fever, shaking chills, profuse sweating.

Non-inflammatory pleural syndromes:

2.1 Hydrothorax is an accumulation of non-inflammatory effusion (transudate) in the pleural cavity.

Pathophysiological mechanisms of hydrothorax:

Increased hydrostatic pressure in the pulmonary capillaries - with heart failure, hypervolemia, difficulty in venous outflow;

Reduced colloid-oncotic pressure of blood plasma - with nephrotic syndrome, liver failure;

Impaired lymphatic drainage – vena cava syndrome, tumors of the pleura, mediastinum.

2.2 Chylothorax- This is an accumulation of lymph in the pleural cavity.

Damage to the thoracic lymphatic duct during surgical interventions, chest injuries;

Blockage of the lymphatic system and veins of the mediastinum by a tumor or metastases;

2.3 Hemothorax- This is an accumulation of blood in the pleural cavity.

Possible causes of hemothorax:

1) wounds and injuries of the chest;

2) rupture of an aortic aneurysm;

3) iatrogenic – with catheterization of the subclavian vein, translumbar aortography, uncontrolled treatment with anticoagulants;

4) spontaneous bleeding in patients with hemophilia, thrombocytopenia.

The clinical manifestations of hydrothorax, chylothorax and hemothorax are caused by the presence of pleural effusion and correspond to those in the syndrome of exudative pleurisy. However, there are distinctive signs: the absence of intoxication syndrome; with hemothorax - manifestations of posthemorrhagic anemia.

2.4 Pneumothorax syndrome is a pathological condition caused by the presence of air in the pleural cavity.

Clinical manifestations of pneumothorax syndrome:

Complaints:

1) pain in the chest - occurs suddenly with coughing, physical stress, intensifies with deep breathing;

2) inspiratory dyspnea, occurs suddenly;

3) non-productive cough.

Sometimes pneumothorax is asymptomatic and is a diagnostic finding during X-ray examination.

General inspection. With the rapid development of pneumothorax, the patient takes a forced sitting position, the skin is moist, cold, pale due to reflex collapse.

Examination of the chest. The affected half is increased in volume and lags behind in the act of breathing. Tachypneous. Reducing chest excursion.

Percussion of the lungs: There is a tympanic sound above the area of ​​pneumothorax, the lower border of the affected lung is raised, the mobility of the lower pulmonary edge is limited.

Auscultation of the lungs: weakening or absence of vesicular breathing and bronchophony. On the affected side, manifestations of lung collapse syndrome can be detected.

Cardiovascular research: swelling of the neck veins, frequent, small, thread-like pulse, tachycardia, displacement of the apical impulse and the boundaries of relative dullness of the heart to the healthy side.

2.4 Fibrothorax syndrome is a pathological condition caused by obliteration (fusion) of the pleural cavity. Fibrothorax is formed as a result of conditions such as hemothorax, pleural empyema, tuberculosis, and chest surgery.

Clinical manifestations of fibrothorax:

Complaints:

1) shortness of breath;

2) periodic pain in the chest, aggravated by deep inspiration, physical activity, and changes in weather conditions.

Chest examination: the affected half is reduced in volume, respiration lags behind, and chest excursion is limited.

Percussion– dull sound, decrease in the height of the apexes and the width of the Krenig fields, the lower border of the affected lung is raised, the mobility of the lower pulmonary edge is reduced.

Auscultation of the lungs– weakening of vesicular respiration.

State budgetary educational institution

higher professional education

"Orenburg State Medical University"

Ministry of Health of the Russian Federation

Department of Propaedeutics of Internal Diseases

PULMONARY SYNDROMES

Orenburg - 2006

Inflammatory infiltration syndrome of pulmonary tissue……..	4
Lung air cavity syndrome…………………………..	7
Bronchial obstruction syndrome…………….	9
Syndrome of increased airiness of lung tissue…………..	12
Syndrome of fluid accumulation in the pleural cavity.........	14
Syndrome of air accumulation in the pleural cavity…………...	17
Atelectasis syndrome…………………………………………….	20
Respiratory failure……………………………………	23
Adult respiratory distress syndrome……………………	29
Literature…………………………………………………………	31

INFLAMMATORY SYNDROME

The severity of symptoms in compacted pulmonary tissue syndrome depends on the size, localization and spread of infiltration (focal or lobar (lobar) pneumonia). Lobar infiltration of lung tissue is characterized by stages: Stage I (initial, “tide” stage); II – stage of compaction (red and gray hepatization); III – stage of resolution.

Infiltrate with destructive changes in the lung tissue can subsequently lead to persistent pathological changes in the form of sclerosis, i.e. the alveoli are filled with connective tissue (pneumosclerosis, lung carnification).

Lung tissues are infiltrated with neoplasm cells - tumor infiltration; blood - in case of pulmonary infarction
Complaints. Cough– dry at the beginning of the development of pulmonary infiltration, with sputum (productive) due to the formation of exudate in the alveoli and hypersecretion of mucus in the bronchi. The sputum can be mucopurulent, bloody (influenza pneumonia), “rusty” in case of lobar pneumonia in the red hepatic stage.

Hemoptysis– occurs with pulmonary infiltrates with destructive phenomena (pulmonary tuberculosis, bronchoalveolar lung cancer).

Dyspnea– occurs when large pulmonary infiltrates form. It is caused by restrictive ventilation disorders, a decrease in the respiratory surface of the lungs. Dyspnea is usually mixed.

Spirometry reveals restrictive ventilation disorders - decreased vital capacity of the lungs.

On electrocardiogram There may be a deviation of the electrical axis of the heart to the right, an increase in the amplitude of the P wave in leads II and III.

Hydropneumothorax – the presence of both gas and liquid in the pleural cavity. In this case, percussion in the lower sections (the place of fluid accumulation) reveals a dull sound, and higher (above the air) a tympanic percussion sound. On auscultation, there is a sharp weakening or absence of vesicular breathing. When the position of the patient’s body changes, you can listen to the “symptom of a falling drop,” and when the patient’s body shakes, you can hear the sound of Hippocrates splashing. Radiographically, gas produces a brighter field, while liquid produces a dark field with a clear boundary.
ATELECTASIS SYNDROME
Atelectasis is a pathological condition of the lung or any part of it, in which the pulmonary alveoli do not contain air, as a result of which their walls collapse. Dyselectasis is a condition in which the air capacity of the lung tissue is significantly reduced.

Atelectasis can be congenital (detected in a newborn) and acquired (secondary collapse of the alveoli of a previously breathing lung). Acquired atelectasis, according to the mechanism of formation, can be obstructive, compression, distension (functional atelectasis - occurs due to violations of the conditions for expansion of the lung during inspiration in bedridden patients, after anesthesia, with ascites, severe chest pain) and mixed.

According to the prevalence, atelectasis can be total, lobar, segmental, lobular and discoid.

OBTURATORY ATELECTASIS (OA) – caused by complete or partial (dyselectasis) closure of the bronchial lumen. Causes of obstructive atelectasis: aspiration of a foreign body, blockage of the bronchial tube with mucus, viscous sputum, endobronchially growing tumor. In the area of ​​collapse of the lung tissue, congestive plethora develops, and edematous fluid leaks into the lumen of the alveoli.

Complaints. Paroxysmal dry cough. With a lung tumor – hemoptysis.

Dyspnea– its severity depends on

the speed of development of bronchial obstruction.

Inspection. There is rapid breathing, diffuse cyanosis, puffiness of the face, a decrease in volume (retraction) of the affected half of the chest and a lag in the act of breathing. With total OA, the chest becomes flatter and narrower on the affected side, the intercostal spaces narrow and retract, and the ribs may overlap each other. The shoulder on the side of atelectasis drops, and the spine bends with a convexity towards the healthy side.
Palpation. Rib cage in the field of OA Regidna. Voice tremors over the affected area of ​​the lung absent or weakened(the voice does not extend through the obstructed bronchus to the area of ​​atelectasis).

Percussion. With topographic percussion, the lower border of the lung on the side of atelectasis is determined higher than on the healthy side. The mobility of the pulmonary edge decreases on the losing side. The percussion sound over the OA becomes shortened or dull (because the lung tissue becomes denser). An absolutely dull lung sound occurs when lung tissue is replaced by an airless environment.

Auscultation. There is a sharp weakening of vesicular respiration over the OA area.
Instrumental methods. X-ray There is a uniform darkening of the corresponding parts of the pulmonary field, and with total atelectasis - of the entire lung. The atelectatic lobe appears darkened and reduced in volume. Atelectasis on a radiograph looks like a wedge-shaped or triangular shadow, with its apex directed towards the root and its base towards the surface of the lung. The shadow of the mediastinum shifts towards the lesion.

Bronchography reveals a defect in the filling of the bronchus, erosion of its contour.

COMPRESSION ATELECTASIS (CA) (“lung collapse”) – develops as a result of external compression of the lung tissue with the accumulation of a large amount of fluid or air in the pleural cavity, with large-scale pathological processes in the chest cavity (aneurysm, tumor of the pleura or mediastinum).

Complaints. CA is characterized by symptoms of the underlying disease (see syndromes of fluid and air accumulation in the pleural cavity).
Inspection. With CA, unlike OA, there may be smoothing or bulging of the intercostal spaces and a lag of the affected half of the chest in the act of breathing (due to the main cause of atelectasis - fluid or air in the pleural cavity).
Palpation. Vocal tremors over the coronary artery region are enhanced (voice sound flows freely through the freely traversed bronchus into the atelectatically compacted lung tissue).

Percussion. Percussion reveals a dull sound. The mediastinal organs are shifted towards the healthy lung, since with CA on the affected side the intrapleural pressure is increased.

Auscultation. By auscultation, bronchial breathing can be heard over the coronary artery region (the airless, compacted lung tissue of the coronary artery region conducts sound waves well to the surface of the chest). In case of incomplete CA (diselectasis), crackling, moist rales are heard over its area (formed as a result of the release of respiratory bronchioles during inhalation, which are compressed by the surrounding tissue during exhalation). Bronchophony over the coronary artery region is enhanced.
RESPIRATORY FAILURE
Respiratory failure (RF) is a pathological condition of the body in which either the maintenance of normal blood gas composition is not ensured, or it is achieved through increased work of the external respiration apparatus. With DN, the partial tension of oxygen in arterial blood (PaO₂) is 45 mm Hg.

DN can occur in various pathological processes in the body, and in pulmonary pathology, DN is the main clinical and pathophysiological syndrome. The pathogenesis of DN in lung diseases is most often caused by dysfunction of the external respiratory apparatus. Mechanisms for the development of DN: disruption of alveolar ventilation, diffusion of molecular oxygen and carbon dioxide through the alveolar capillary membrane, disruption of blood perfusion through the pulmonary capillaries.

Violations of alveolar ventilation, depending on the mechanisms causing these disturbances, are divided into obstructive, restrictive and mixed.

Obstructive respiratory failure occurs due to narrowing of the airways (obstruction) and increased resistance to air movement. It is usually caused by spasm of the bronchi or their local damage (tumor in the bronchus, granulation, cicatricial stenosis, inflammatory or congestive edema of the bronchial mucosa, etc.).

Restrictive type of breathing disorder is caused by a decrease in the respiratory surface of the lungs or a decrease in their extensibility (restrictio - restriction, decrease). Restrictive DN is observed in acute and chronic massive inflammatory processes and congestion in the lungs (pneumonia, tuberculosis, chronic heart failure), with the accumulation of fluid and air in the pleural cavity, with pulmonary emphysema, with massive obstacles to the expansion of the chest (kyphoscoliosis).

Mixed type of ventilation impairment is characterized by the presence of signs of both obstructive and restrictive ventilation disorders.

Classification of respiratory failure

(Dembo A.G., 1962)

1. 
   According to etiology:

primary DN– caused by damage to the external respiratory apparatus itself;

secondary DN– caused by pathology of other parts of the respiratory system (circulatory organs, blood, tissue respiration).

1. 
   According to the rate of formation of clinical and pathophysiological manifestations:

acute DN– a violation of gas exchange in which the flow of oxygen into the blood and the removal of carbon dioxide from the blood stops, which often ends in asphyxia (cessation of breathing);

chronic DN– characterized by a gradual increase in gas exchange disturbances and tension in compensatory processes, which are manifested by hyperventilation and increased blood flow in unaffected lung tissue. The time frame for the development of chronic DN is months and years.

1. 
   According to changes in blood gas composition:

latent DN– not accompanied by disturbances in the blood gas composition at rest;

partial DN– characterized by arterial hypoxemia or venous hypercapnia;

global DN– characterized by arterial hypoxemia and venous hypercapnia.
The main manifestation of DN is dyspnea– a feeling of lack of air and the associated need to increase breathing. Objectively, shortness of breath is accompanied by changes in the frequency, depth, rhythm of breathing, as well as the duration of inhalation and exhalation. Shortness of breath is caused by excitation of the inspiratory center, which spreads to the periphery to the respiratory muscles and to the overlying parts of the central nervous system. Shortness of breath Shortness of breath is often accompanied by feelings of fear and anxiety.

Depending on the phase of breathing, inspiratory dyspnea is distinguished, which is characterized by difficulty in inhaling; expiratory - exhalation is difficult and mixed, in which the inhalation and exhalation phases are difficult.

The second important clinical sign of DN is central cyanosis– bluish coloration of the skin and mucous membranes, due to the high content of reduced hemoglobin in the blood (more than 50 g/l, with the norm being 30 g/l). Central (pulmonary) cyanosis is characterized by a diffuse, ash-gray skin tone (detected during private examination), while the skin is warm on palpation. In acute DN, cyanosis can develop in a few seconds or minutes; in chronic DN, cyanosis develops gradually.

Acute respiratory failure

Causes: aspiration of a foreign body and obstruction of the upper respiratory tract, sudden bronchospasm (severe attack of suffocation or asthmatic condition), extensive atelectasis or inflammation of the lungs, pulmonary edema, acute suffocation as a result of dysfunction of the respiratory center, respiratory muscles and blood circulation, compartment syndrome, severe mechanical damage, massive bleeding.

There are three stages in the development of acute DN:

Istage (initial)– patients are characterized by a forced position – orthoptic, rapid breathing up to 40 per minute with the participation of auxiliary respiratory muscles, pronounced cyanosis of the skin and visible mucous membranes, signs of dysfunction of the central nervous system (irritability, agitation (anxiety or euphoria), sometimes delirium, hallucinations ). Physical examination methods correspond to the pathology that caused acute DN. Many patients have respiratory sounds audible at a distance. Auscultation in the lungs can detect “mosaic” breathing (breathing is not audible in the lower parts, and hard in the upper parts with a moderate amount of dry and wet rales). There is tachycardia up to 120 beats per minute, a moderate increase in blood pressure and symptoms of acute right ventricular failure - swelling of the neck veins and enlargement of the liver.

Blood gas composition: moderate arterial hypoxemia (PaO₂ 60-70 mm Hg) and normocapnia (PaCO₂ 35-45 mm Hg).

IIstage (deep hypoxia)– the condition of the patients is extremely serious: severe shortness of breath, shallow breathing, patients convulsively gasp for air. The forced position remains. Periods of excitement are replaced by indifference, drowsiness, lethargy, sometimes convulsions, involuntary urination and defecation occur. Auscultation above the lungs over a large area on both sides may not be able to hear respiratory sounds (“silent lung”), and only in small areas can breathing and wheezing be heard. There is increasing decompensation from the cardiovascular system: rapid pulse (up to 140 per minute), weak filling, muffled heart sounds, a gallop rhythm is possible, low blood pressure.

Blood gas composition: severe arterial hypoxemia (PaO₂ 50-60 mm Hg) and hypercapnia (PaCO₂ 50-70 mm Hg). Acid-base balance study - respiratory acidosis.

IIIstage (hypercapnic coma)– no consciousness, diffuse diffuse cyanosis, cold sweat. Breathing is shallow, infrequent, non-rhythmic, areflexia, mydriasis (dilated pupils). On auscultation of the lungs, respiratory sounds are absent or sharply weakened. The pulse is threadlike, arrhythmic; blood pressure is sharply reduced or not determined; Heart sounds are dull, often gallop rhythm, ventricular fibrillation is possible.

Blood gas composition: severe arterial hypoxemia (PaO₂ 40-55 mm Hg) and pronounced hypercapnia (PaCO₂ 80-90 mm Hg). Study of acid-base balance - metabolic acidosis. Soon, asphyxia (cessation of breathing), cardiac arrest and death occur.

Pathogenetically, acute respiratory failure is distinguished between hypoxemic and hypercapnic. Hypoxemic or parenchymal (pulmonary) DN is characterized by hypoxic hypoxemia, which is difficult to correct with oxygen therapy. It can occur against the background of severe pneumonia, pulmonary edema, and acute respiratory distress syndrome in adults.

Hypercapnic or ventilatory (“pumping”) DN is characterized by hypercapnia, and hypoxemia is also present, but responds well to oxygen treatment. This type of acute DN develops due to dysfunction of the “respiratory pump” and the respiratory center. The most common causes of hypercapnic DN are chronic obstructive pulmonary disease, respiratory muscle dysfunction, obesity, kyphoscoliosis, etc.

Chronic respiratory failure

Causes: chronic respiratory diseases.

Chronic DN develops gradually over months and years. The timing of its development depends on the rate of severity and the degree of disruption of the processes of ventilation of the alveoli, diffusion of gases and blood perfusion. As DN progresses, the work of the respiratory muscles at rest increases, the volumetric velocity of blood flow and redistributive vascular reactions increase to increase the amount of oxygen, the metabolism and the body's need for oxygen increases. As a result, a moment comes when maintaining the blood gas composition even at rest becomes impossible and tissue hypoxia, hypercapnia and gas acidosis develop.

There are 3 stages or degrees of chronic DN. One of the main criteria for dividing into degrees is shortness of breath in combination with cyanosis and other symptoms that are caused by chronic hypoxemia and tissue hypoxia.

I– compensated (hidden, latent) chronic DN (occurs without hypoxemia) – with increased physical activity, the respiratory rate increases to 26-28 per minute, and at rest does not exceed 20; heart rate – 68-85 per minute. During exercise, increased fatigue and sometimes cyanosis are noted. All symptoms disappear after a short rest.

II– subcompensated (pronounced)– characterized by moderate hypoxemia. Breathing at rest is 20-25 per minute, its depth can be reduced, shortness of breath increases with minor physical activity. Signs of heart failure are observed: the pulse is increased, the liver is enlarged by 2-3 cm, and sometimes swelling of the lower extremities. Fatigue and cyanosis are more pronounced, and the pulse quickens. Symptoms disappear after prolonged rest.

III– decompensated (pulmonary-cardiac)– compensatory mechanisms cannot normalize changes in respiration and hemodynamics. There is constant shortness of breath at rest - 30 breaths per minute or more, shallow breathing. Characterized by attacks of suffocation, pronounced cyanosis, constant tachycardia at rest (100 heartbeats per minute). There is circulatory failure.

Additional clinical signs of chronic DN are secondary erythrocytosis, increased blood viscosity, increased hematocrit and blood hemoglobin concentration, capillary stasis, right ventricular hypertrophy, hypoxic damage to parenchymal organs.

RESPIRATORY DISTRESS SYNDROME IN ADULTS
Respiratory distress syndrome (RDS) in adults is one of the types of acute respiratory failure that occurs during acute lung injury with the development of non-cardiogenic pulmonary edema, impaired external respiration and hypoxia.

RDS syndrome can develop in various acute processes: severe bacterial or viral pneumonia, sepsis, aspiration of gastric contents, prolonged shock, oxygen intoxication, blood transfusion, acute hemorrhagic pancreatitis.

Under the influence of any etiological factor, the alveolar-capillary membrane is damaged, vascular permeability to high-molecular proteins increases and non-cardiogenic pulmonary edema develops.

Pathological picture: Acute lung injury leads to activation of blood cells. Activated leukocytes and platelets accumulate in the capillaries of the lungs, interstitium and alveoli and release cytotoxic substances that induce the development of fibrosis and also change the reactivity of the bronchi and blood vessels. Damage to the endothelium of the pulmonary capillaries and alveolar epithelium leads to increased vascular permeability, resulting in plasma and blood leaking into the interstitial and alveolar spaces. The alveoli fill with fluid, which causes atelectasis. The phenomena of developing fibrosis lead to low lung compliance, pulmonary hypertension and hypoxemia.
Complaints. Questioning such patients is difficult due to their serious condition. Anamnesis is collected from the words of relatives or people around the patient. There may be complaints of shortness of breath and severe general weakness.
Inspection. A detailed picture of RDS syndrome becomes obvious within 24-48 hours.

The general condition of the patients is severe or extremely serious. Consciousness may be depressed or absent. The patient's position is passive. Upon examination, severe shortness of breath and shallow breathing are revealed. The skin is pale in combination with cyanosis. Possible “spotting” of the skin.

Physical examination methods are generally not specific.

Auscultation. Weakened vesicular breathing, moist and multiple dry rales are heard above the surface of the lungs. Sometimes the auscultatory picture remains normal.

C-m respiratory failure

C-cavity formation in the lungs

C-m accumulation of air in the pleural cavity (pneumothorax)

S-th accumulation of fluid in the pleural cavity (hydrothorax)

S-m compaction of lung tissue

S-m pulmonary heart

With increased airiness of the lungs

C-m inflammatory obstruction of small bronchi

C-m inflammatory lesions of the tracheo-bronchial tree

S-m intoxication and nonspecific inflammatory changes

Intoxication syndrome (nonspecific)

Observed in all inflammatory diseases:

Increased body temperature

Weakness, malaise, weakness

Decreased appetite

Increased fatigue, sweating

Pain, aches in the body and muscles

Headache

Impaired consciousness (euphoria, agitation, delirium)

General inflammatory changes in the blood (leukocytosis, accelerated ESR, shift of the leukocyte formula to the left, positive CRP, increased fibrinogen content, increased alpha-2 and gamma globulins in the blood serum)

Lung compaction syndrome

1. Inflammatory infiltration of the lungs

2. Atelectasis of the lung

3. Local pneumofibrosis

4. Carnification of the lung

5. Tumor

This is both a nonspecific inflammatory process and specific inflammation (infiltrative pulmonary tuberculosis with edema) with exudation in the alveoli.

Typical objective data

Sometimes Sternberg's positive sm is on the losing side

Dullness or dullness to percussion

Harsh or bronchial breathing

Adverse respiratory sounds (moist rales, pleural friction noise, crepitus)

Atelectasis of the lung

AL is a violation of airiness as a result of collapse of the lung or part of it, due to the cessation of air access to the alveoli due to blockage or compression of the bronchus itself (enlarged lymph node, large amount of exudate in the pleural cavity)

Pathogenesis - when ventilation of areas of the lung ceases and while its blood supply is maintained, air is absorbed from the lung distal to the site of blockage, which causes collapse of the lung tissue or the lung is compressed from the outside.

A.L. - can be obstructive and compression

Obstructive atelectasis

Bronchial tumor

Foreign body

Compression of the bronchus from outside

Blockage of discharge (mucus, sputum)

Respiratory movements in this area of ​​the chest are limited.

With the duration of A.L. For more than 3 months, there is a retraction of part of the chest (due to a decrease in intrapulmonary pressure).

RG-uniform shading, with greater A. the median shadow (heart, large vessels) is shifted towards the lesion.

Compression atelectasis

Compression of the lung from outside (effusion into the pleural cavity, bleeding, etc.).

The area of ​​lung tissue above the fluid level is compressed and collapses, but bronchial patency is maintained.

In this case, a strip of lung tissue is determined above the fluid level, above which sound phenomena are heard characteristic of compaction of the lung tissue by the type of inflammatory infiltration (increased vocal tremor, dullness of percussion sound, harsh or bronchial breathing).

There are no adverse breath sounds.

Local fibrosis

It is detected in the lung tissue at the site of frequent repeated inflammation.

Objectively - manifested by all phenomena characteristic of tissue compaction, with the exception of adverse respiratory sounds

Carnification (a pathological process in which the pulmonary parenchyma changes its physical properties, acquiring the consistency and appearance of meat)

Most often, the outcome is pneumonia, when the inflammatory exudate (usually rich in fibrin) does not resolve, but is organized by sprouting connective tissue.

Objectively – manifested by all phenomena characteristic of compaction of lung tissue, with the exception of adverse respiratory sounds

Lung tumor

Peripheral cancer

Bronchial cancer (atelectasis often develops)

Objectively – all the signs characteristic of pulmonary tissue compaction syndrome (adverse respiratory sounds may also appear)

Pneumonia

Acute P. - acute exudative inflammatory processes of different etiology and pathogenesis, localized in the parenchyma and interstitial tissue of the lung, often involving the vascular system in the process.

Pulmonary parenchyma - respiratory bronchioles, alveolar ducts, alveolar sac, alveoli

Etiology of pneumonia

Infectious factor - bacteria, viruses, rickettsia, mycoplasma, chlamydia, legionella, fungi, etc.

Non-infectious factors

Chemical (petrol) – drivers

Physical (radiation)

Secondary infection

Pathogenesis of pneumonia

P. are divided into primary and secondary.

Primary - arise as independent diseases in a person with previously healthy lungs in the absence of diseases of other organs and systems.

Secondary – complicating other diseases (chronic bronchitis, congestive heart failure, postoperative, enzymatic (pancreatitis), autoimmune (collagenosis)

Microorganisms enter the lungs

Bronchogenic

Hematogenous

Lymphogenic

Airborne

Contagious (from nearby lesions - subhepatic abscess, mediastenitis)

Provoking factors

Smoking, Alcohol, Old age, Surgeries, Hypothermia, Viral infections

Classification of pneumonia -2

Moscow (1995) - 5th National Congress on Respiratory Diseases

Community-acquired

Intrahospital (hospital, nosocomial - more than 72 hours)

Atypical - caused by intracellular “atypical” pathogens (legionella, mycoplasma, chlamydia)

Pneumonia in patients with immunodeficiency conditions

Classification of pneumonia - 1

By etiology (bacterial, viral, due to physical and chemical factors, mixed

By pathogenesis (primary, secondary)

According to clinical and morphological characteristics (parenchymatous - lobar, focal, large-, small-focal, confluent, interstitial)

By location and length

Unilateral, bilateral (total, lobar, segmental, sublobar, central, basal)

By severity (mild, moderate, severe, extremely severe)

Along the course (acute, prolonged - more than 6 weeks)

Pathogens of pneumonia

1.Gr+ microorganisms:

Pneumococci (str. Pneumoniae) 70-96%, the most aggressive serotypes of pneumococci 1,2,3,6,7,14,19

Staphylococcus aureus (staph.aureus) 0.5-5%. With epidemic outbreaks up to 40%, a tendency to destruction

Pyogenic streptococcus (strep.pyogenes) 1-4%, during an influenza epidemic, complications of pleurisy, pericarditis are common

2.Gr- microorganisms:

Friedlander's bacillus (Klebsiella pneumoniae) 3-8%. Found in the oral cavity, sick after 40 years of age, severe course, viscous bloody sputum, confluent lesion, most often the upper lobe, foci of decay in the lung tissue, purulent complications

Escherichia coli (Escherichiae coli) 1-1.5%, for diabetes mellitus, confluent, in the lower sections).

Proteus (p. rettgeri, h. vulgaris, p. mirabilis, p. morgagni). In alcoholics, the upper lobe, decay.

Afanasyev-Pfeiffer bacillus (Hemophilus influenzae) 1-5%. Lives in the nasopharynx, during an influenza epidemic, with bronchitis, bronchiectasis, the lower lobe with involvement of the pleura

Pseudomonas aeruginosa (Pseudomonas aeruginosa) 3-8%. The causative agent of nosocomial infection, with concomitant glucocorticoid, cytostatic therapy

Legionella (Legionella pneumophille) 1.5%. Opening year 1976. Air-conditioned premises. Sometimes combined with diarrhea, high fever, acute renal failure.

3. Anaerobic pathogens (isolated cases, foul-smelling sputum)

4. Protozoa (Pneumocystis), HIV-infected patients, in weakened patients, after transplantation, with immunodeficiency, radiation therapy. The stages of the course are edematous, atelectatic, emphysematous stages. Romanovsky-Giemsa smears (pneumocystis)

5. Viruses (influenza, parainfluenza, respiratory syncytial, cytomegalovirus - during suppressive therapy, after transplantation)

6. Mycoplasma. More often in groups of people, discrepancy between severe intoxication, catarrhal symptoms and symptoms of lung damage

7. Chlamydia. Enlarged liver, lymph nodes, normal spleen, signs of pneumonia

8. Legionella.

Croupous (pleuropneumonia, lobar) pneumonia

KP is an acute inflammatory process of the pulmonary parenchyma involving a segment or lobe of the lung, which is based on a hyperergic inflammatory reaction, manifested by filling the alveoli with fibrin-rich exudate.

Etiology– pneumococci types 1-3.

Stages (path anatomy)

1st stage – high tide. Hyperemia of the lung tissue, inflammatory edema, 12 hours - 3 days.

Stage 2 – red liver, 1-3 days. The area of ​​inflammation is airless, dense, red in color with graininess on the cut.

Stage 3 – gray hepatization, 2-6 days. Neutrophils accumulate in the alveoli. The lung is gray-green in color.

Stage 4 – permits.

Clinic of lobar pneumonia

The onset is sudden, acute

Terrific chills

High fever, febris continua

Pleural pain on the affected side

Intoxication syndrome, “delirium tremens” - delirium tremens

Cough – dry at first, after 24 hours the sputum is “rusty”, scanty, viscous

Objectively – dullness, harsh or bronchial breathing, pleural friction noise, crepitao indux et redux

Lab. data – leukocytosis, shift to the left, accelerated ESR, toxic granularity of neutrophils, changes in the protein spectrum of the blood

Focal pneumonia (bronchopneumonia)

Acute AP is an acute inflammatory process of the pulmonary parenchyma involving a lobule or group of lobules.

Peculiarities pathogenesis acute AP

Volume of lesion (one or more lobules, segment, multiple foci)

Inflammation from the small bronchi spreads to the lung parenchyma (with lobar inflammation it spreads through the alveolar tissue through the Kohn pores)

An immediate hypersensitivity reaction in the respiratory area is not typical

Characteristic involvement of the bronchi in the inflammatory process

Impaired airway patency (possible microatelectasis)

The pleura is involved in the inflammatory process only when the inflammation is located superficially in the lungs

Morphological changes are not characterized by stages

The sputum is mucopurulent, serous (with CP there is a lot of fibrin)

Clinical features

Gradual onset of the disease (after ARVI)

Chest pain is rare (with a superficial location of the inflammation)

Cough from the very beginning with phlegm

Symptoms of intoxication are less pronounced

Shortness of breath is less common

Dullness of percussion sound is less pronounced

Breathing is often weakened vesicular

Wet fine rales (rarely pleural friction noise, crepitus is not observed)

The appearance of bronchophony is not typical

Syndrome of inflammatory changes of the tracheobronchial tree

Clinically presented by cough, sputum production. Hard breathing, dry wheezing.

Small bronchial obstruction syndrome

Reversible obstruction - inflammatory swelling of the bronchial mucosa - accumulation of viscous secretion, bronchospasm

Irreversible - narrowing of the bronchial lumen due to diffuse development of peribronchial sclerosis

Causes of bronchial obstruction – bronchitis, bronchospasm

Clinic of bronchial obstruction

Expiratory dyspnea

Extended exhalation

Dry wheezing on exhalation

Cough with difficult sputum

Development of emphysema

Bronchitis

Acute bronchitis– acute inflammation of the bronchial mucosa, characterized by an increase in bronchial secretion and clinically manifested by cough, and in some cases shortness of breath (with damage to the small bronchi)

Etiology

Infectious factors

Allergic factors

Chemical, physical factors (smoke, vapors of acids, alkalis, gases, etc.)

Pathogenesis– disturbance in the functioning of the mucociliary apparatus of the bronchi

Associated factors - unfavorable weather conditions (high humidity, cold air), smoking, alcoholism, decreased immunity, impaired mucociliary transport

Classification (by level of damage)

Tracheobronchitis (trachea and large bronchi)

Bronchitis (segmental bronchi)

Bronchiolitis (small bronchi, bronchioles)

Clinic

Cough, often paroxysmal, painful

First dry, then mucopurulent sputum

When the larynx is involved - barking

Slight rise in temperature

Objectively

Box shade of percussion sound

Breathing is harsh over the entire surface, dry wheezing (wet only when the smallest bronchi are involved)

Chronical bronchitis:

Diffuse, progressive damage to the bronchial tree, characterized by restructuring of the secretory apparatus of the mucous membrane, as well as sclerotic changes in the deeper layers of the bronchial walls and peribronchial tissue

CB - persons who have a cough with sputum for at least 3 months a year for 2 years in a row, excluding other diseases with such symptoms

The main criteria for chronic disease

Diffuse nature of the lesion of the bronchial tree both along the length and deep into the wall

Progressive course with periods of exacerbations and remissions

The dominant symptoms are cough, sputum, shortness of breath

Etiology

Infection

Atmospheric pollution (sulfur dioxide, pollutants, acid vapors, etc.)

Heredity (deficiency of ά1-antitrypsin, secretory Ig A)

Pathogenesis

Combination

Excess mucus production (hypercrinia)

Changes in the normal composition of the secretion (discrimination) and its viscosity

Mucociliary transport disorders

All these factors lead to the accumulation of secretions in the bronchial tree

Forms of chronic bronchitis

Chronic (simple) non-obstructive bronchitis– predominantly the proximal (large and medium) bronchi are affected, with a relatively favorable clinical course and prognosis. Clinical manifestations are a constant or intermittent cough with sputum production. Signs of bronchial obstruction only during periods of exacerbation and in the later stages.

Chronic obstructive bronchitis– along with the proximal and distal bronchi are affected. Clinically – cough, steadily increasing shortness of breath, decreased tolerance to physical activity.

Classification of chronic bronchitis

1.Form of CB – simple (non-obstructive), obstructive

2. Clinical, laboratory and morphological characteristics - catarrhal, mucopurulent, purulent

3. Phase of the disease - exacerbation, clinical remission

4. Severity – mild (FEV1-more than 70%), moderate (FEV1-from 50 to 69%), severe (FEV1-less than 50%)

5.Complications of chronic disease - pulmonary emphysema, DN (chronic, acute, acute on the background of chronic), bronchiectasis, secondary pulmonary hypertension, cor pulmonale (compensated, decompensated)

6.Primary CB and secondary CB (as a syndrome of other diseases, such as tuberculosis)

Chronic non-obstructive bronchitis

1. Damage to the bronchial mucosa by tobacco smoke, pollutants, repeated infections

2. Hyperplasia of goblet cells of the bronchial glands and hyperproduction of bronchial secretions (hypercrinia) and deterioration of the rheological properties of mucus (discrinia)

3. Violation of mucociliary clearance, protective and cleansing function of the bronchial mucosa

4. Focal degeneration and death of ciliated cells with the formation of “bald” spots

5. Colonization of damaged mucosa by microorganisms and initiation of a cascade of cellular and humoral inflammatory factors

6. Inflammatory edema and formation of areas of hypertrophy and atrophy of the mucosa

Clinic

1. Cough with mucous or mucopurulent sputum

2. Increased body temperature to subfebrile levels

3.Mild intoxication

4.Hard breathing

5.Dry scattered wheezing

6. At the height of exacerbation, symptoms of broncho-obstruction are possible due to the accumulation of viscous sputum in the bronchi and bronchospasm

7. In the remission phase, a cough with sputum is detected, there is no shortness of breath

Pathogenesis of chronic obstructive bronchitis

1. Inflammatory process in all bronchi (especially small ones)

2. Development of broncho-obstructive syndrome (combination of reversible and irreversible components)

3.Formation of pulmonary emphysema (centroacinar emphysema - due to early damage to the respiratory parts of the lungs - damage to the central part of the acinus)

4. Progressive impairment of pulmonary ventilation and gas exchange - leads to hypoxemia and hypercapnia

5. Formation of pulmonary arterial hypertension and chronic pulmonary heart disease

Clinic of chronic obstructive bronchitis

1. Expiratory shortness of breath, aggravated by physical activity and coughing

2. Boring, unproductive cough

3.Lengthening the expiratory phase

4.Secondary emphysema

5. Scattered dry wheezing (with quiet and forced breathing) and distant wheezing

Complications of chronic bronchitis

1.Infection related

Secondary pneumonia

Bronchiectasis

Infectious-allergic bronchial asthma

2. Associated with disease progression

Diffuse pneumofibrosis

Emphysema

Respiratory failure

Pulmonary heart

Chronic obstructive pulmonary disease

COPD is a disease characterized by irreversible bronchial obstruction, which has a progressive course and is associated with inflammation of the airways that occurs under the influence of unfavorable environmental factors (smoking, occupational hazards, pollutants). Its main symptoms are cough with sputum production and shortness of breath.

COPD is a heterogeneous group (COPD, emphysema, asthma, bronchiolitis obliterans, cystic fibrosis, bronchiectasis.

The unifying feature is inflammation of the mucous membrane of the respiratory tract, a violation of the ventilation function of the obstructive type.

Signs of exacerbation of COPD(Anthonisen et al.,1987 criteria)

1.Increase in sputum volume

2. Appearance of purulent contents in sputum

3. Appearance or progression of shortness of breath

Three types of exacerbations(important for assessing severity and treatment)

First - all three signs are present

Second - there are two signs

Third - there is one sign

Etiology and pathogenesis of COPD-1

Risk factors

Tobacco smoking (deterioration of mucociliary transport, decrease in the cleansing and protective function of the bronchi, promotes chronic inflammation of the mucous membrane, negative effect on surfactant - decrease in the elasticity of the lung tissue)

Occupational hazards (cadmium, silicon dust) – miners, builders, railway workers, workers associated with the processing of cotton, grain, paper

Respiratory viral infections

Hereditary predisposition

Etiology and pathogenesis of COPD-2

Risk factor – impact on the bronchial mucosa, interstitial tissue and alveoli – formation of a chronic inflammatory process – activation of neutrophils, macrophages, mast cells, platelets. Neutrophils – release of cytokines, prostaglandins, leukotrienes – formation of chronic inflammation.

The formation of pulmonary emphysema due to the destruction of the elastic framework of the lung tissue. The main cause of destruction is an imbalance in the “protease-antiprotease” and “oxidant-antioxidant” systems due to the pathogenic functioning of neutrophils.

A shift in the ratio of damage and repair processes, which are regulated by pro-inflammatory and anti-inflammatory mediators.

Impaired mucociliary clearance - colonization of mucous microflora - activation of neutrophils - increased destruction. Centroacinar and panacinar pulmonary emphysema is formed.

Emphysematous type of COPD

“Shortness of breath” - “pink puffing”. Symptoms of CB are less pronounced than the morphological and functional signs of emphysema. Asthenics and people of short stature predominate. Increased airiness due to the valve mechanism - “air trap”. Panacinar emphysema. At rest, there are no disturbances in the ventilation-perfusion relationship, and the normal gas composition of the blood is maintained. During physical activity there is shortness of breath and PaO2 decreases. Advanced DN, arterial hypertension and cor pulmonale develop late. Patients “puff”, puffing out their cheeks, there is no cyanosis for a long time, cor pulmonale – hence the name “pink puffers”.

Bronchitic type of COPD - “bluish edematous”

Centroacinar emphysema. Classic manifestations of COB. Hypersecretion of mucus, swelling of the mucous membrane, bronchospasm - increased resistance to inhalation and exhalation - arterial hypoxemia and shortness of breath, increased PaCO2, the occurrence of hypercapnia. Pulmonary hypertension and cor pulmonale develop earlier than in the emphysematous type. Dry wheezing, prolonged exhalation, cyanosis, peripheral edema are heard - the patient has “cyanotic edema”

Bronchial asthma

BA is a chronic relapsing disease, the obligatory pathogenetic mechanism of which is altered bronchial reactivity as a result of specific immunological (sensitization + allergy) or nonspecific mechanisms. The main clinical sign is an attack of suffocation due to bronchospasm and swelling of the bronchial mucosa.

Pathogenesis of asthma

Altered bronchial reactivity - disruption of narrowing/expansion processes, increased mucus production, disruption of its evacuation

Main pathogenetic variants BA

Exogenous (atopic, allergic)

Endogenous (non-atopic, non-allergic)

Aspirin BA

Autoimmune

Exercise asthma

Cholinergic variant of asthma

Night asthma

Cough variant of asthma

Professional BA

Dishormonal (hypoglucocorticoid deficiency, hyperestrogenism)

Neuropsychic (hysterical, neurasthenic, hypochondriacal)

Adrenergic imbalance (predominance of ά-adrenergic receptors over β-adrenergic receptors

Primary disorders of bronchial reactivity

BA Clinic

Attacks of suffocation of the expiratory type, which is based on bronchospasm + the appearance of viscous “vitreous” sputum

Three periods of suffocation

Precursors of suffocation (sneezing, dry nose, dry cough, vasomotor rhinitis, Quincke's edema)

The height of the attack (expiratory type suffocation, short inhalation and prolonged exhalation, wheezing, dry non-productive cough, forced position of the body with support on the hands, signs of DN (cyanosis, shortness of breath, changes in blood gases - PO2↓, PCO2), impaired venous outflow ( puffiness of the face), objective signs of bronchospasm

Reversal (cough with glassy sputum)

Complications of asthma

Pulmonary – status asthmaticus, emphysema, DN, pneumothorax

Extrapulmonary – cor pulmonale, heart failure

Asthmatic status - criteria

Progressive impairment of bronchial obstruction (severe asthma attack, worsening heart failure, diffuse cyanosis)

Rigidity to bronchodilators

Hypercapnia

Hypoxemia

Stages of status asthmaticus

Stage 1 – prolonged attack of asthma (dissonance between wheezing heard at a distance (there are many of them) and determined by a phonendoscope during auscultation (there are fewer of them)

Stage 2 – a more severe condition of the patient, DN, “silent lung” - lack of breathing over a particular area or the entire lung

Stage 3 – development of a comatose state “red cyanosis” - hypercapnia, hypoxemia, acidosis

Mortality 20%

Emphysema

EL is a pathological expansion of air spaces distal to the terminal bronchioles, accompanied by destructive changes in the respiratory bronchioles and alveoli as a result of the pathogenic action of neutrophils accumulating in the intercellular space (definition of the American Lung Association)

Pulmonary heart syndrome

LS is a clinical syndrome caused by hypertrophy or dilatation of the right ventricle resulting from hypertension of the pulmonary circulation due to bronchial diseases, chest deformation or damage to the pulmonary vessels.

Acute drugs– 90% PE, pulmonary hypertension develops within a few hours

Subacute drugs– recurrent pulmonary embolism occurs over several weeks, months, repeated attacks of asthma

Chronic drug– occurs over several years

Pathogenesis of drugs

The basis of drugs is hypertension in the pulmonary circulation and the development of alveolar hypoxia. The Euler-Lillestrand reflex is important (increased tone of the pulmonary vessels in response to alveolar hypoxia), which leads to an increase in blood pressure in the pulmonary circulation - the pulmonary heart is formed

Clinic LS

Main lung disease + heart failure of the right ventricular type

Compensated LS = clinical picture of the underlying disease + right ventricular hypertrophy and/or right ventricular dilatation

Decompensated LS = clinical picture of the underlying disease + right ventricular hypertrophy and/or right ventricular dilatation + symptoms of cardiac right ventricular failure (swelling of the jugular veins, enlarged liver, edema, ascites)

Fluid in the pleural cavity

Pleural effusion is the accumulation of excess fluid in the pleural cavity, caused by inflammation of the pleura, impaired blood and lymph circulation, increased permeability of non-inflammatory capillaries, pleural tumors or other reasons.

1. Pleurisy (accumulation of exudate)

2.Hydrothorax (accumulation of transudate)

Cirrhosis of the liver

Hypoproteinemia in NS

Heart failure

3. Hemothorax (collection of blood)

4. Chylothorax (lymph accumulation)

Pleurisy

P – inflammation of the pleura, often with the formation of fibrinous plaque on its surface and effusion in the pleural cavity.

Pleurisy – dry (fibrinous) and effusion (exudative)

allergic (drug and other allergies, allergic alveolitis)

autoimmune (Dresler syndrome, rheumatism, rheumatoid arthritis, SLE, dermatomyositis, scleroderma)

post-traumatic (trauma, thermal, chemical, radiation damage)

Factors causing effusion

Increased secretion of inflammatory exudate into the pleural cavity

Microcirculation disorders, decreased resorption

Formation of fibrin film and connective tissue - decreased reabsorption of pleural fluid

Pleurisy clinic

Dry pleurisy (fibrinous)

Pneumonia

Pulmonary tuberculosis

Viral infection

Purulent-inflammatory processes in the lungs

1. Chest pain

2.Dry painful cough

3. Increased body temperature

4.Mussy's sign (sensitivity when pressing pressure points)

5.M.b. weakened vesicular breathing

6. Pleural friction noise (audible on inhalation and exhalation, increases with pressure with a stethoscope, does not change when coughing)

Exudative (exudative) pleurisy

Usually begins with fibrinous P.

Reduces chest pain

Signs of respiratory failure increase

Displacement of the mediastinum and trachea to the healthy side

Diffuse gray cyanosis

Expansion of the chest on the affected side, its lag in the act of breathing (Hoover's symptom), the intercostal spaces are smoothed (Litten's symptom), the skin fold on the affected side is more massive than on the healthy side (Wintrich's symptom)

Dullness (dullness) of percussion sound

The difference between exudate and transudate