Inflammatory infiltration of the lungs. Syndrome of inflammatory infiltration of lung tissue Suppurative diseases of the lungs


observed with lobar pneumonia, focal pneumonia, pulmonary tuberculosis and is characterized by an acute onset, high fever, chills, pain in chest 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 superficial. From the 2nd day there is no a large number of mucous viscous sputum, sometimes containing streaks of blood. Quite quickly, the sputum acquires a brown-reddish color (“rusty” sputum), which is due to the decay products of red blood cells from the areas of red hepatization. The amount of sputum discharge increases, but does not exceed 100 ml per day. In the stage of gray hepatization and especially the resolution of the disease, 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 side of the lesion, cyanosis of the lips, acrocyanosis, herpetic eruptions on the lips, cheeks and wings of the nose quite often appear. Quite often, when breathing, a wide movement of the wings of the nose is noted. 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.
With percussion of 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, acquires the character of a pronounced dullness (femoral tone). Voice trembling at the beginning of the disease is somewhat increased, and in the stage of hepatization it becomes clearly enhanced.
During auscultation, at the beginning of the disease, breathing is weakened vesicular, and in the second stage it becomes bronchial. In the first days of the disease, in some cases, cripitatio indues are detected, scattered dry and moist rales can be heard in a small amount. When the process spreads to the pleura, a pleural friction rub 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, hallucinations can be observed. There are also changes in other organs and systems: tachycardia, lowering blood pressure, sometimes up to collapse, accent II tone over pulmonary artery. Elderly and old individuals may develop signs of heart and coronary insufficiency, sometimes heart rhythm disturbances.
An x-ray examination of the lungs reveals a homogeneous darkening of the corresponding lobe or segment. In the study of blood: neutrophilic leukocytosis up to 20 - 109 l, shift to the left up to 6 ~ 30% of stab neutrophils. There is also relative lymphopenia. 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 erythrocytes. In the stage of resolution, the state of health improves, coughing decreases, muffling of percussion sound, breathing becomes hard, and then turns into vesicular, during this period, crypitation (crepitacio redux), sonorous fine bubbling rales, the number of which gradually decreases.
NURSING DIAGNOSIS: fever, chills, chest pain, cough with mucopurulent or rusty sputum. Plan of examination, treatment and care of the patient.
IMPLEMENTATION OF THE PLAN: the nurse prepares the patient for an x-ray examination, takes biological material (blood, sputum) for laboratory testing, performs medical appointments for the treatment of the patient (distributes medicines in a timely manner, makes various injections and infusions), prepares the patient for consultation of specialists (oncologist , phthisiatrician) according to indications, provides care for the patient (ventilation of the ward, 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), performs the setting of mustard plasters and cans, etc.
LUNG ABSCESS SYNDROME is a severe process that proceeds with severe intoxication, accompanied by necrosis and melting of the lung tissue with the formation of cavities. The abscess syndrome in the lung proceeds in two stages: the stage of infiltration or abscess and the stage of the cavity. 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, the addition of an infection, and a decrease in reactivity
macroorganism. The abscess syndrome is characterized by persistent or hectic fever, chills with profuse sweating, pain on the affected side, dry cough, but if chronic bronchitis accompanies, there may be a small amount of mucous or mucopurulent sputum. Quite often, symptoms of intoxication are observed: general weakness, malaise, loss of appetite, headache. An objective examination of the patient may reveal lagging of the affected half of the chest during breathing, weakened voice trembling over the C1 abscess, weakened vesicular breathing, with accompanying bronchitis, dry buzzing rales can be heard, with ^ percussion over the abscess, dullness or dull percussion sound.X-ray examination reveals a rounded 4 shadow with clear edges.Blood examination: leukocytosis up to 20 ¦ 109 l, shift of the leukoformula to the left to metamyelocytes, increased ESR 3. A sharp increase in the amount of purulent sputum discharge (up to 500-1000 ml) with a fetid odor indicates a breakthrough [of the abscess in the bronchus and its release. t
Sputum may show blood streaks. At the same time, the condition of the patients improves, the body temperature decreases, the chills disappear and the symptoms of intoxication decrease. It should be noted (attention is drawn to the fact that sputum is secreted more with a certain J position of the patient (drainage occurs). Physical examination reveals increased voice trembling, tympanic, percussion sound, bronchial breathing, may 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 coarse or medium bubbling rales may be heard. An x-ray examination reveals a rounded enlightenment with clear edges, if a secret remains in the cavity, then a blackout area with a horizontal level is determined. When examining blood, leukocytosis and increased ESR persist, but with a downward trend. Sputum examination reveals a significant amount of leukocytes and elastic fibers.
NURSING DIAGNOSIS: fever, chills, chest pain, malaise, headache, cough with purulent sputum.
PLAN for examination, treatment, care and observation: preparation of the patient for X-ray examination, for laboratory examination, fulfillment of medical prescriptions for the treatment of the patient (timely distribution medicines, production of injections and infusions), organization of other methods of treatment (physiotherapy, exercise therapy, massage, oxygen therapy), organization of care and monitoring of the patient.
IMPLEMENTATION OF THE PLAN: timely and targeted fulfillment of prescriptions (antibiotics of various spectrums of action, sulfonamides, nitrofurans, nystatin or levorin, mucolytics). Timely collection of biological material (blood, sputum, urine) for laboratory testing. Organization of a consultation with a physiotherapist for the appointment of physiotherapeutic methods; exercise therapy doctor for the appointment of exercise therapy and massage. Organization of timely ventilation of the ward, wet cleaning with disinfectants, washing and disinfection of the spittoon, timely change of underwear and bed linen, prevention of bedsores, regular rotation of the patient to create drainage and sputum discharge - 4-5 times a day for 20-30 minutes; monitoring the activity of the cardiovascular system (pulse, heart rate, measurement of blood pressure), bronchopulmonary system (respiratory rate, amount of sputum), physiological functions.
SYNDROME OF THE PRESENCE OF LIQUID IN THE PLEURAL
CAVITIES (exudative pleurisy) - is an inflammatory lesion of the pleura, accompanied by the accumulation of fluid in the pleural cavity. development inflammatory process in the pleura contributes to the exacerbation of the tuberculous 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 (abdominal and typhus), rheumatism, collagenosis, lung tumors. The provoking factor, as a rule, is hypothermia. This syndrome is characterized by inflammation of the pleural sheets and, first of all, by the deposition of fibrin on them. By the nature of the fluid in the pleural cavity, pleurisy can be serous-fibrinous, hemorrhagic, purulent, chylous and mixed. In the presence of fluid in the pleural cavity of a non-inflammatory or unknown origin, they speak of a pleural effusion.
The disease begins gradually or acutely, with high temperature, severe stabbing pains in the chest, aggravated by deep inspiration or bending to the healthy side and coughing. The cough is usually dry and painful. The examination reveals the forced position of the patient on the affected side, shortness of breath, cyanosis, lagging of the affected side of the chest during breathing. With the accumulation of fluid, patients feel a feeling of heaviness, dull pain on the affected side; if a lot of fluid accumulates, then there may be a shift of the mediastinum to the healthy side and severe shortness of breath appears. The fluid, as a rule, is located along a parabolic curve (Damoiseau lines), its top is located along the posterior axillary line. In this regard, three zones are distinguished: the zone of preloaded

lung to the root (Garland's triangle), the zone of hydrothorax and the zone of displaced mediastinum to the healthy side (Rauhfus-Grokko's triangle). With physical research methods in the area of ​​the compressed lung (compression atelectasis), palpation is determined by increased voice trembling and bronchophony, tympanitic-tympanic percussion sound, auscultatory-bronchial breathing. In the zone of hydrothorax: voice trembling and bronchophony, as well as breathing are not determined, femoral tone is determined percussion. The same is determined in the zone of mediastinal displacement (Rauhfus-Grocko 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, fulfilling medical prescriptions for treatment and consulting a phthisiatrician and an oncologist. In the implementation of the PLAN IMPLEMENTATION, great importance is given to preparing the patient for an x-ray examination, taking biological material for laboratory testing, preparing the patient for pleural paracentesis, and accurately fulfilling medical prescriptions in treating the patient: timely distribution of drugs and injections. X-ray examination is determined by the blackout on the affected side with an oblique level of fluid.
Pleural puncture (pleural paracentesis) is of great diagnostic and therapeutic value. 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 forceps, a 50 ml Janet syringe, dishes for collecting pleural 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 bedk in it, the density of the pleural fluid are determined, and a Rivalta test is performed to detect exudate or transudate. The main principles of treatment are the appointment of anti-inflammatory and anti-tuberculosis drugs, general tonic, vitamin therapy, after the evacuation of the pleural fluid to prevent the adhesive process, exercise therapy and physiotherapy are prescribed after consulting a physiotherapist.
CHOKING SYNDROME. Most often, this syndrome is caused by a disease such as bronchial asthma. By bronchial asthma is meant an allergy with a predominant localization of hyperergic inflammation in the bronchopulmonary apparatus, 24

characterized by recurrent, predominantly generalized, airway obstruction, reversible in early stages diseases. There are bronchial asthma atopic (non-infectious-allergic) and infectious-allergic. In atopic asthma, the cause can be any substance that can cause the formation of antibodies in the human body. Allergens can be animal and plant origin, as well as chemicals with a simple and complex structure.
In the infectious-allergic form, the cause of the development of bronchial asthma is the microbial flora. In addition, the etiological factors in the development of bronchial asthma are psychogenic, climatic (hypothermia, insolation) factors, as well as pronounced physical activity. Moreover, these factors, as a rule, are provocative and can sometimes be trigger points for the development of asthma. Clinical manifestations: the leading clinical symptom complex of bronchial asthma is expiratory dyspnea, 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 asthma attack upon contact with an allergen. The cessation of exposure to the allergen also causes the cessation of the attack. At the same time, suffocation, as a rule, is preceded by an aura, which is distinguished by a pronounced polymorphism of manifestations ( vasomotor rhinitis with copious separation of watery secretions, migraine, urticaria, pruritus, sore and sore 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. Aura in patients of this group in most cases is expressed by cough. Attacks are usually moderate or severe, quite long and resistant to conventional therapy, often transforming into an asthmatic condition. The most commonly found sensitivity to staphylococcal toxin and streptococcus. Main clinical symptoms an attack of suffocation are expiratory shortness of breath against the background of limited chest mobility (low diaphragm), wheezing, scattered dry whistling and buzzing rales, constantly changing their intensity and localization. The patient always takes the forced position of orthopnea 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, on the part of the cardiovascular system, tachycardia, deafness of heart tones, the boundaries of absolute cardiac dullness are not determined due to 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 delayed, then there is a pronounced depression sick, pallor skin is replaced by warm cyanosis of the skin of the face and extremities, as a result of developing tissue hypoxia in the heart, anginal pains may occur. During a pronounced attack of suffocation, fractures of those ribs to which the anterior scalene and external oblique muscles are attached can be noted. Their opposite action during coughing can cause a rib fracture. Possible formation of spontaneous pneumothorax, interstitial or mediastinal emphysema. Enough serious complication is the occurrence of acute emphysema, as well as a ‘large emphysematous cyst (bulla). During physical examination, it is noted: palpation of the resistance of the chest, weakening of voice trembling; percussion - box tone, significant limitation of mobility of the pulmonary edge and omission of the lower border of the lungs; auscultatory - weakened vesicular breathing, a lot of dry whistling, less often buzzing rales.
NURSING DIAGNOSIS: shortness of breath with prolonged exhalation, cough, dry cup, tachycardia, cyanosis.
PLAN for monitoring and caring for the patient, preparing the patient for additional methods research, sampling of biological material (blood, sputum) for laboratory research, fulfillment of medical prescriptions for the treatment of a patient, provision of pre-medical emergency care preparing the patient for consultation with other specialists.
IMPLEMENTATION OF THE PLAN OF ACTIVITIES nurse. First of all, the nurse must provide the first first aid during 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 fresh air, give oxygen, put mustard plasters, give a warm drink, report to the attending or on-call doctor and then follow the doctor's prescriptions . In the study of peripheral blood at the height of the attack, eosinophilia and basophilia are detected. In the study of sputum, a triad is characteristic: an increased content of eosinophils, the presence of Charcot-Leiden crystals and Kurshman spirals. When examining the function external respiration in patients at the height of an asthma attack, a decrease in VC is detected, the residual volume and functional residual capacity increase significantly. An important feature are pronounced violations of bronchial patency.
PRINCIPLES OF TREATMENT: etiological therapy in atopic form of bronchial asthma is possible when an allergen is detected. It is necessary to eliminate the allergen from the patient's everyday life, adherence to a diet that excludes allergenic products, and hygiene measures when patients are sensitive to house dust. If it is impossible to eliminate the allergenic factor, it is necessary to conduct specific or non-specific desensitizing therapy. A contraindication to desensitizing therapy is the presence of pulmonary tuberculosis, pregnancy, decompensated cardiosclerosis, decompensated rheumatic heart disease, thyrotoxicosis, decompensated diseases of the kidneys, liver, mental illness, severe pulmonary insufficiency.
Acute bronchitis syndrome, or acute bronchitis, is a fairly common disease of the respiratory system. Most often acute inflammation bronchi is observed in patients with acute respiratory diseases caused by influenza, parainfluenza, adenovirus infection, as well as severe forms measles, whooping cough, diphtheria. Quite often there are acute bronchitis caused by bacterial agents against the background of exposure to the influenza virus, which inhibits phagocytosis and leads to the activation of the bacterial flora of the respiratory tract. In the sputum of such patients, influenza bacillus, pneumococci, hemolytic streptococcus, Staphylococcus aureus, Friedlander's wand, etc. 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 acute bronchitis. Other causes of acute bronchitis include inhalation of air containing high concentrations of nitrogen oxides, sulfuric and sulfurous anhydride, hydrogen sulfide, chlorine, ammonia, bromine vapor, as well as in case of damage by chemical warfare agents (chlorine, phosgene, diphosgene, mustard gas, lewisite, FOB ). Enough common cause acute bronchitis can be inhalation of air with a high content of dust, especially organic.
CLINICAL MANIFESTATIONS: the appearance of a dry, irritating cough, a feeling of soreness or pain behind the sternum, then the process passes to large and small bronchi, which leads to symptoms of airway obstruction (paroxysmal cough, shortness of breath). On the 2-3 day, mucous or mucopurulent sputum begins to separate, sometimes with an admixture of blood. Most patients have pain in the lower chest, caused by coughing and convulsive contraction of the diaphragm, general weakness, malaise, weakness, pain in the back and limbs, 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 often the temperature rises to 39 ° C and above, while heipes labialis, hyperemia of the mucous membranes of the pharynx and pharynx, often with pinpoint hemorrhages, are often detected.
Percussion - pulmonary sound. During auscultation in the first days of the disease, vesicular breathing with an extended expiration is determined, scattered dry whistling and buzzing rales, when coughing, the number of rales changes. After 2-3 days, wet rales of various sizes usually join. From the side of the cardiovascular system, tachycardia, from the side nervous system- headache, weakness, poor sleep.
NURSING DIAGNOSIS: cough, malaise, weakness, shortness of breath, tachycardia, fever, poor sleep.
PLANNING nursing interventions: care and observation, examination and fulfillment of medical prescriptions for the treatment of patients.
IMPLEMENTATION OF THE PLAN of nursing actions: independent - methods of care and monitoring of the patient: pulse rate, respiration, heart rate, measurement of blood pressure, physiological functions, general condition, ventilation of the room, setting mustard plasters, cans;
dependent - taking biological material (blood, urine, sputum) for laboratory testing, preparing the patient for a chest X-ray, examining the function of external respiration, timely distribution of drugs, administration medicines parenterally. Blood tests revealed leukocytosis of 8109 l, accelerated ESR; in sputum a significant amount of microflora; when examining the function of external respiration, a decrease in VC and maximum ventilation is detected; when small bronchi are involved in the process, a violation of bronchial patency and forced vital capacity is detected; X-ray examination sometimes shows an expansion of the shadow in the root of the lungs. A consultation with a physiotherapist is organized to prescribe physiotherapeutic treatment (electrophoresis with potassium iodide, calcium chloride, aminophylline, etc., exercise therapy).
PRINCIPLES OF TREATMENT: treatment is often carried out at home, where the patient must avoid sudden changes in ambient temperature. From drugs - anti-inflammatory media

properties: amidopyrine, analgin, aspirin, which have antipyretic and analgesic effects.
In severe acute bronchitis during an influenza epidemic, in the elderly and old people, as well as debilitated patients, it is advisable to hospitalize and prescribe tableted antibiotics and sulfonamides in general doses.
To liquefy sputum, infusions of thermopsis, ipecac, infusions and extracts of marshmallow root, mukaltin, 3% potassium iodide solution, alkaline inhalations, exercise therapy are prescribed. In the presence of bronchospasm, bronchodilators are prescribed: tablets of theofedrine, ephedrine, 0.025 g each, and eufilin, 0.15 g each, 3 times a day.
With a dry painful cough, you can prescribe: codeine, dionine, hydrocodone, libexin, baltic. Distractions are prescribed: mustard plasters on the chest and back, cans, warm foot baths, plentiful warm drinking, taking mineral waters alkaline content.
To prevent the transition of acute bronchitis to chronic complex therapy, it should be continued until the patient has fully recovered.
CHRONIC BRONCH INFLAMMATION SYNDROME is
chronic bronchitis, which is a diffuse inflammation of the mucous membrane of the bronchial tree and deeper layers of the bronchial wall, characterized by a long course with periodic exacerbations. According to the definition of WHO experts, "patients with chronic bronchitis include persons who have a cough with sputum for at least three months a year for two years, with the exclusion of other diseases of the upper respiratory tract, bronchi and lungs that could cause these symptoms." This is a fairly common disease of the broncho-pulmonary system, it should be noted the tendency to increase the incidence. More often people over the age of 50 get sick, and men get sick 2-3 times more often.
The factors contributing to the occurrence of chronic bronchitis should be considered, first of all, the constant irritation of the mucous membranes of the respiratory tract by polluted air. Importance at the same time, they also have unfavorable climatic conditions: a damp climate with frequent fogs and a sharp change in weather. Irritation of the mucous membranes of the respiratory tract by dust or smoke, especially tobacco, is a trigger for increased production of mucus in the respiratory tract, which leads to coughing and sputum production, easier infection of the bronchial tree. Chronic bronchitis occurs 3-4 times more often among smokers than non-smokers. big
importance in the etiology of chronic bronchitis is given to exposure to occupational hazards - in workers of woolen and tobacco factories, flour and chemical plants, miners, miners. Of no small importance is the pollution of large cities with sulfur dioxide, acid fumes, vehicle exhaust gases, and smoke particles.
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). Accession of 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 sown from sputum or bronchial contents, less often Pseudomonas aeruginosa, Friedlander's bacillus. The frequency of exacerbations of chronic bronchitis increases dramatically during periods of influenza epidemics. Currently, certain importance is attached to the factors of hereditary predisposition to the development of chronic processes in the broncho-pulmonary system.
CLINICAL MANIFESTATIONS: The most frequent and main symptoms of chronic bronchitis are cough (dry or wet), sputum of various amounts and nature, impaired pulmonary ventilation and bronchial patency. Most patients, usually smokers, have a slight cough for several years, dry or with mucus sputum, mainly in the morning, which patients do not attach importance to. Gradually, the cough becomes more pronounced, causes inconvenience, increases in cold and damp weather, after hypothermia, infections of the upper respiratory tract and is accompanied by periodic separation of mucopurulent or purulent sputum. In the initial period of the disease, large bronchi are affected. Violation of bronchial patency in this case is expressed slightly, 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, a violation of bronchial patency occurs ( obstructive bronchitis) with the development of shortness of breath. Initially, shortness of breath is disturbing physical activity, then becomes constant. Its severity increases during periods of exacerbation. In patients with a predominant lesion of the small bronchi, in addition to shortness of breath, there is cyanosis and paroxysmal cough, which worsens when moving from a warm room to a cold one. Natural during obstructive bronchitis is the development of emphysema and chronic cor pulmonale.
At any stage of the disease, the addition of a bronchospastic syndrome, characterized by the development of expiratory dyspnea, can be observed. Cases where bronchospasm is leading to clinical picture diseases and at the same time there are signs of allergies (vasomotor rhinitis, drug or food allergy, blood eosinophthia, the presence of eosinophils in sputum), it is customary to refer to asthmatic bronchitis. During periods of exacerbation of the disease, an increase in body temperature is observed, more often to subfebrile numbers, general weakness, sweating, fatigue, pain in various muscle groups associated with their overexertion when coughing.
Percussion sound at the beginning of the disease is little changed, but with the development of emphysema, a box sound is determined, a decrease in the mobility of the lower edges of the lungs.
During auscultation during the remission of the disease, breathing can be vesicular or, in the presence of emphysema, weakened vesicular breathing is heard. In some areas, breathing can be hard, with a small amount of wheezing. During the period of exacerbation, dry or moist rales are heard, the number of which can vary widely. In the presence of bronchospasm against the background of an elongated exit, dry whistling rales are heard, the number of which increases with forced breathing.
NURSING DIAGNOSIS: cough dry or wet, shortness of breath, malaise, fatigue, sweating, fever.
PLAN examination, care and observation, principles of treatment.
IMPLEMENTATION OF THE PLAN: independent - methods of care and observation of the patient are used; dependent - taking biological material (blood, urine, sputum) for laboratory testing, preparing patients for X-ray examination, bronchoscopy, timely distribution of drugs, injections and infusions as prescribed by a doctor. A blood test revealed 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 research there may be an increase in the content of fibrinogen, sialic acids, C-reactive protein
In the study of sputum in patients with asthmatic bronchitis, eosinophils, Charcot-Leiden crystals, Kurshman spirals can be detected. An X-ray examination determines a taut pulmonary pattern, in the presence of emphysema - an increase in the transparency of the lung 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, cylindrical and saccular bronchiectasis.
PRINCIPLES OF TREATMENT: in case of exacerbation of the disease, treatment should be carried out in a hospital. Treatment must be comprehensive. The main component during periods of exacerbation is antibiotic 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, levorin are used. To restore the drainage function, expectorants are used (infusion of thermopsis, marshmallow root in the form of infusions and extracts), a 3% solution of potassium iodide is a very effective expectorant; in the presence of viscous sputum, enzymes (trypsin, chemotrypsin, chymopsin, ribonuclease, etc.) are used in the form of aerosol inhalations. Only with a dry, hacking, debilitating cough should codeine be used. The best discharge of sputum is facilitated by inhalation of alkaline solutions, plentiful hot drinking, and the intake of alkaline mineral waters. When bronchospasm is prescribed: ephedrine, novodrine, etc. One of the components complex therapy are desensitizing and antihistamine drugs (diphenhydramine, suprastin, pipolfen, calcium gluconate, aspirin, etc.). With persistent bronchospasm, corticosteroid therapy is indicated. In severe exacerbations, an important place belongs to therapeutic bronchoscopy, in which the bronchi are washed with Ringer's solution, furagin or soda with the removal of purulent contents, casts of the bronchi, plugs and the introduction of drugs (antibiotics, hormones, enzymes) into the bronchial tree, when the process subsides - physiotherapy procedures (sollux, UVI, UHF currents, electrophoresis with novocaine, calcium chloride on the chest, exercise therapy).
SYNDROME OF INCREASED AIR LUNG TISSUE (emphysema). The term "emphysema" (from the Greek emphysae - to inflate, inflate) denotes 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 pulmonary bloating (prolonged cough, overstrain of the external respiratory apparatus in glass blowers, 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 a1-antitrypsin. With a lack of the latter, there is a decrease in the protection of the mucous membranes of the bronchial tree and lung parenchyma from the damaging effect 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 may be interstitial or alveolar. Interstitial emphysema is characterized by the penetration of air into the stroma of the lung (peribronchial, perilobular), often combined with mediastinal emphysema, subcutaneous emphysema. More common is alveolar emphysema with increased air content in the alveoli. Alveolar emphysema may be diffuse or limited.
The most common form - alveolar diffuse emphysema - is a consequence of chronic obstructive pulmonary disease. In the presence of obstruction during exhalation, breathing is difficult and occurs mainly due to the additional work of the respiratory muscles. Violations of ventilation processes develop during each respiratory act, there is a decrease in intra-alveolar oxygen tension and an increase in carbon dioxide tension. Violation of intraalveolar ventilation causes increased stretching of the alveoli, contributes to the loss of elasticity of the interalveolar septa. Stretching of the walls of the alveoli leads to difficulty in blood flow to the adjacent

Pathologically, pulmonary infiltration refers to the penetration into lung tissues and the accumulation of cellular elements, fluids and various chemical substances. Impregnation of lung tissues only with biological fluids without admixture of cellular elements characterizes pulmonary edema, and not infiltration.

The syndrome of pulmonary infiltration consists of characteristic morphological, radiological and clinical manifestations. In practice, this syndrome is diagnosed most often on the basis of clinical and radiological data. Morphological examination (biopsy) is carried out if a more in-depth examination of the patient is necessary.

In pathology, infiltration of the lungs 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 inflammatory infiltrate is played by other components of the connective tissue - interstitial substance, fibrous structures.

Leukocyte inflammatory infiltrates

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, transient (for example, acute inflammatory) infiltrates usually resolve and do not leave noticeable traces. An infiltrate with significant destructive changes in the lung tissue in the future most often gives persistent pathological changes in the form of sclerosis, a decrease or loss of lung function.

Lymphoid (round cell), lymphocytic plasma cell, macrophage infiltrates

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 may be a manifestation of extramedullary processes of hematopoiesis, such as lymphocytic infiltrates.

Tumor infiltration

Lung tissues are infiltrated with hematopoietic cells. In such cases, one speaks of tumor infiltration, or infiltrative tumor growth. Tumor cell infiltration leads to atrophy or destruction of the lung tissue.

X-ray signs of pulmonary infiltration

Infiltration is characterized by a moderate increase in the volume of lung tissue, its increased density. That's why radiological signs pulmonary infiltration have their own characteristics. So, for example, inflammatory infiltration is inherent irregular shape shading and uneven outlines. AT acute stage darkening contours are not sharp, gradually pass into the surrounding lung tissue. Plots 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 gaps of the air-filled bronchi.

Infiltration of the lungs is the process of replacing the lung tissue with normal airiness by an area with increased density and increased volume, containing cellular elements unusual for this tissue (leukocytes, lymphocytes, macrophages, eosinophils, etc.). This syndrome consists of characteristic morphological, radiological and clinical signs.

What diseases occurs

The most common cause of infiltration in the lungs is pneumonia.

The lung tissue infiltration syndrome can be a manifestation of various pathological conditions. The most common infiltrate in the lungs is formed in the following diseases:

  1. Inflammatory processes in the lungs of various nature:
  • viral;
  • bacterial;
  • fungal;
  • congestive pneumonia;
  • hypostatic pneumonia, etc.
  1. Respiratory damage with.
  2. Anomalies of development:
  • (pathological fistula between the arteries and veins of the lung);
  • sequestration of the lung (part of the lung tissue is separated from the bronchi, pulmonary blood vessels and is supplied with blood from the arteries extending from the aorta);
  • (disembryonic formation, consisting of elements of the lung parenchyma and bronchial wall).
  1. Allergic infiltrate in the lungs.
  2. or benign neoplasms.
  3. Focal pneumosclerosis.

How does it manifest

The clinical picture with lung infiltration is due to the disease that caused the pathological process. The severity of symptoms depends on the area of ​​the lesion and the general reactivity of the organism. But there are general manifestations of this syndrome, characteristic of any diseases that occur with the formation of infiltrate in the lungs. These include:

  • complaints of cough, hemoptysis, pain in the chest (with damage to the pleural sheets);
  • change in general condition (fever, intoxication);
  • objective data: lag of half of the chest in the act of breathing (on the "sick" side), increased voice trembling and dullness of percussion sound over the pathological focus, weakening of respiratory noises in this area, less often dry and wet rales during auscultation;
  • X-ray data: limited or diffuse darkening of the lung field.

Below we dwell on the features of the infiltration syndrome in the most common pathological conditions.

Infiltration in pneumonia

The inflammatory process in the lungs can be caused by a large number of various pathogens, and therefore its course has certain differences.

  • Staphylococcal differs from other inflammatory processes in the lungs by a tendency to destructive changes with the formation of cavities.
  • Pneumonia caused by Klebsiella occurs in debilitated patients or the elderly. It can occur with mild intoxication, cough with bloody sputum with the smell of burnt meat. Already on the first day, the collapse of the lung tissue in the affected area is possible with the formation of thin-walled cystic cavities.
  • With anaerobic pneumonia, microabscesses form in the focus of infiltration, which, merging with each other, break into the bronchus, which leads to the release of fetid sputum with a cough. Often, their breakthrough occurs towards the pleura and patients develop empyema.
  • Candidal pneumonia is characterized by a sluggish course with repeated relapses, migration of pneumonic foci and the formation of effusion in the pleural cavity.
  • The incidence of influenza pneumonia increases dramatically during the epidemic. Clinical course it varies from mild forms to death. The disease proceeds with characteristic symptoms (fever, pain in eyeballs, muscles, adynamia, runny nose). Then joins paroxysmal cough with sputum mixed with blood, shortness of breath. In the lungs, uneven blackouts are detected in the form of foci or affecting the entire lobe of the lungs. Later, nausea, vomiting, and mental disorders may appear.

The classical course of the syndrome of infiltration of inflammatory genesis can be traced on the example of croupous (lobar) pneumonia.

This pathology is caused, as a rule, by pneumococci and has an acute onset. The patient suddenly has the following complaints:

  • high body temperature (up to 39-40 degrees);
  • chills;
  • severe general weakness;
  • labored breathing;
  • unproductive cough;
  • chest pain on coughing and deep breathing.

During this period, swelling of the walls of the alveoli and the accumulation of inflammatory exudate in their lumen are observed in the lungs, and the elasticity of the lung tissue decreases. An objective examination reveals typical signs of infiltration of the lung tissue and additionally crepitus of the “tide” during auscultation.

Gradually, the alveoli are completely filled with pathological secretions, and the cough becomes wet with sputum that is difficult to separate, sometimes rusty in color. The lung tissue in the affected area becomes dense and resembles the density of the liver. The auscultatory picture changes - bronchial breathing is heard above the pathological focus. General state patients can be severe, some of them have impaired consciousness.

Timely treatment started in most patients quickly leads to a decrease in intoxication and a decrease in body temperature. In the resolution phase of the process in the focus, inflammation decreases and the exudate gradually resolves. At the same time, patients are concerned about coughing with sputum of a mucopurulent nature, with auscultation over the surface of the lungs, moist rales (mainly finely bubbling) and “ebb” crepitus are heard.

Aspiration pneumonia also has a severe course. It develops when the acidic contents of the stomach or food enter the lower Airways. This is possible with severe vomiting, reflux esophagitis, during or after anesthesia. A few hours after aspiration, the patient develops:

  • asthmatic shortness of breath;
  • cyanosis;
  • fever;
  • paroxysmal cough;
  • moist rales;

In the future, inflammatory infiltrates are formed in the lungs, which can suppurate.

Clinically, this pathology is manifested by vague symptoms:

  • malaise;
  • slight cough;
  • chest discomfort.

In some cases, it is asymptomatic. On the radiograph, homogeneous blackouts without clear contours are detected, in the blood - a high level of eosinophils. Such infiltrates can be located in any part of the lungs, either disappearing or appearing again.

Usually, the formation of an infiltrate in the lungs is preceded by characteristic symptoms (suffocation, cyanosis, chest pain). On such an infiltrate it has a wedge-shaped shape and faces the root with its apex.

Anomalies of development

The lung tissue infiltration syndrome can be a sign of various developmental anomalies. The latter are most often asymptomatic, so the infiltrate is an accidental finding on the radiograph.

  • Pulmonary sequestration reveals an irregularly shaped opacification or a group of cysts with a perifocal inflammatory response. This pathology can manifest itself with suppuration.
  • If there is a hamartoma in the lungs, an infiltrate with clear contours is found, sometimes with focal calcifications. It is usually located in the thickness of the lung tissue and does not affect the function of the lung tissue. But sometimes the hamartoma is located on the inner surface of the bronchi and can lead to atelectasis and obstructive pneumonia.
  • Arteriovenous aneurysms on the radiograph have the appearance of rounded, clearly contoured opacities, to which dilated vessels approach from the root of the lung. If the discharge of blood exceeds a third of the total volume of blood flowing through the pulmonary circulation, then the person has signs of hypoxemia (weakness, decreased ability to work, shortness of breath, etc.).


Lung infiltration in cancer patients


In lung cancer on the x-ray, the infiltration looks like a blackout with blurry, blurry edges.

Infiltration in the lungs may be associated with malignant or benign tumor processes. They can long time to be latent, revealed only by x-ray examination.

Malignant processes should be suspected if a rapidly growing formation is found on the radiograph, which looks like a blackout with corroded or smeared edges. A particularly high risk of developing this pathology is observed in people with a long smoking history. The first sign of the disease may be an intoxication syndrome; as the tumor grows, characteristic pulmonary symptoms(painful cough, shortness of breath, hemoptysis). When blocked by a growing tumor, the bronchus is formed

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

Morphological (bioptical) examination is carried out if a more in-depth examination of the patient is necessary. Pathologically, pulmonary infiltration refers to the penetration into the tissues of the lung 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 in which pulmonary infiltration syndrome occurs:

In pathology, infiltration of the lungs 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 belongs to other components of the connective tissue - the intermediate substance, fibrous structures.

Leukocyte inflammatory infiltrates are often complicated by suppurative processes (for example, lung abscess), since the proteolytic substances that appear during the release of lysosomal enzymes of polymorphonuclear leukocytes often cause the melting of infiltrated tissues. Loose, short-lived (for example, acute inflammatory) infiltrates usually resolve and do not leave noticeable traces. An infiltrate with significant destructive changes in the lung tissue in the future most often gives persistent pathological changes in the form of sclerosis, a decrease 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 an extramedullary process of hematopoiesis, for example, lymphocytic infiltrates.

Lung tissues are infiltrated with hematopoietic cells. In such cases, one speaks of a tumor infiltration or an infiltrative growth of the tumor. Infiltration by tumor cells leads to atrophy or destruction of the lung tissue.

Symptoms pulmonary infiltration syndromes depend primarily on the disease that causes it, the degree of activity of the inflammatory process, the area and localization of the lesion, complications, etc. The most typical common symptoms pulmonary infiltration is cough, shortness of breath, fever. If the focus of infiltration is located on the periphery of the lung and passes to the pleura, pain in the chest may occur when coughing and deep breathing. In the process of objective examination of patients, rapid breathing, lagging of the interested 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, one can determine the dullness of percussion sound, vesiculobronchial or bronchial breathing, dry and wet rales, crepitus in a limited area of ​​the chest, and increased voice trembling on the side of the lesion.

Infiltration is characterized by a moderate increase in the volume of lung tissue, its increased density. Therefore, radiation signs of pulmonary infiltration have their own characteristics. For example, inflammatory infiltration is characterized by an irregular shape of darkening and uneven outlines. In the acute stage, the darkening contours are not sharp, gradually passing 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 gaps of the air-filled bronchi.

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

Pulmonary infiltration syndrome

The concept of the syndrome of pulmonary infiltration. Causes of infiltration.

Inflammatory and non-inflammatory infiltrates

Tumor infiltrates. Lung cancer in the practice of a general practitioner.

Pulmonary tuberculosis in the practice of a general practitioner. Medical tactics for the examination and treatment of patients.

Differential diagnosis for pulmonary atelectasis

Curation of patients. Analysis of patients.

Pulmonary infiltration syndrome

An infiltrate is a tissue area characterized by an accumulation of cellular elements (inflammatory, eosinophilic, tumor) usually not characteristic of it, increased volume and increased density. In accordance with this, the following main groups of infiltrates in the lungs are distinguished: infectious and inflammatory, for example, with pneumonia and tuberculosis, allergic and infiltrates with tumors (cancerous, leukemic, with malignant lymphomas, etc.).

Differential diagnostic search differs significantly depending on whether the patient has a lobar (segmental, polysegmental) or non-lobar lesion. In this regard, it is advisable to cover differential diagnosis separately for infiltrates of a lobar and non-lobar character.

At the first stage, the doctor must make sure that the patient really has a pulmonary infiltrate. Identification of the infiltrate is carried out according to clinical and radiological data. Depending on the nature of the pulmonary infiltrate (mainly exudative or predominantly productive), there are various physical changes in the lungs. The most striking clinical changes are observed in infectious and inflammatory pulmonary infiltrates, mainly in nonspecific pneumonia: local increase in voice trembling, dullness of percussion sound (or dullness), hard or bronchial breathing, crepitus. With a pulmonary infiltrate of a predominantly productive nature, for example, with tumors, as well as with inflammatory infiltrates with impaired bronchial drainage, increased voice trembling, crepitus and wheezing are not detected, weakened breathing is heard. In such cases, on the basis of clinical data, it is not possible to determine the pulmonary infiltrate.

X-ray examination is of decisive importance for the establishment of pulmonary infiltrate. On the radiograph, the pulmonary infiltrate gives a blackout with a diameter of more than 1 cm of low or moderate intensity, less often, with extensive, for example, lobar, infiltrates, a blackout of considerable density. The contours of the darkening depend on the nature (substrate) of the pathological process, its localization and the projection of the study. The structure of blackout in pulmonary infiltrates can be either homogeneous or heterogeneous, which is determined by the nature of the pathological process, its stage and the presence of complications.

At the second stage of the differential diagnostic search, a distinction is made between inflammatory and tumor infiltrates. Inflammatory infiltrates of a lobar nature are observed mainly in pneumonia and tuberculosis. Infiltrates of a tumor nature usually do not capture an entire lobe. Lobar obscuration in tumors is more often observed in bronchogenic lung cancer, when tumor stenosis of the bronchus leads to hypoventilation and atelectasis of the corresponding segment or lobe, followed by the development of an inflammatory process in these areas (obstructive pneumonitis). Thus, lobar processes in pneumonia and tuberculosis must be differentiated from obstructive pneumonitis.

Obstructive pneumonitis is diagnosed by the presence of clinical and radiological signs of atelectasis (less often hypoventilation) of a lobe or segment in combination with clinical and laboratory signs of an inflammatory process in the lungs. Of great importance for the diagnosis is bronchoscopy with a biopsy of suspicious areas.

Inflammatory infiltrates of a non-lobar character (focal pneumonia, infiltrative pulmonary tuberculosis, allergic processes of the lungs) must be differentiated primarily from peripheral lung cancer, which more often gives an infiltrative shadow of a rounded shape on an x-ray.

Peripheral cancer has an insidious onset, no fever, cough, or shortness of breath, and little or no physical changes in the lungs. AT general analysis blood is determined only by a moderate increase in ESR in the absence of other changes. The main differential diagnostic differences from round-shaped inflammatory infiltrates are determined by X-ray examination. In contrast to peripheral cancer, focal pneumonia usually has an irregularly shaped opacity, which in itself is an important distinguishing feature. In rare cases, the site of homogeneous blackout in focal pneumonia has a rounded shape (spherical pneumonia), while the outer contours of the blackout are fuzzy with a gradual transition to healthy lung tissue. In contrast, in peripheral cancer, inhomogeneous darkening is more often determined with clearer even or wavy contours, on the outer surface of which short linear shadows can be detected that extend into the surrounding lung tissue ("antennae"). Less sharp external contours of the tumor are present in the phase of infiltrating growth, and especially when the underlying disease is complicated by perifocal pneumonia. In such cases, during antimicrobial therapy, a decrease in the size of the darkening is observed, however, a rounded shadow on the radiograph remains. Peripheral lung cancer is prone to decay with the formation of a cavity in the tumor. At the same time, unlike abscessing pneumonia, this cavity is usually located eccentrically and does not contain fluid.

For diagnosis, bronchoscopy is used with aspiration of the contents of the afferent bronchus and its subsequent cytological examination.

Limited non-lobar infiltrates must be differentiated with central lung cancer, uncomplicated atelectasis, giving on the radiograph a picture of an enlarged root with uneven outer contours like "rays of the rising sun" or "janitor's broom", as well as with malignant lymphomas, especially pulmonary lymphogranulomatosis.

At the third stage of differential diagnosis, inflammatory infiltrates are distinguished from each other.

With lobar infiltrates, differential diagnosis is carried out mainly between lobar (often croupous) pneumonia, tuberculous finished off (as a variant of infiltrative pulmonary tuberculosis) and caseous pneumonia.

Tuberculous lobitis and caseous pneumonia have much in common with lobar pneumonia: usually an acute onset, high body temperature, cough, sometimes with bloody sputum, chest pain, similar physical changes in the lungs, x-ray examination - darkening of the lobar character with an increase in the affected lobe. In favor of tuberculous lobitis is evidenced by: 1) heterogeneity of blackout on the radiograph with the presence of denser formations and areas of enlightenment (better visible on the tomogram) and especially focal shadows, both dense and soft due to lymphogenous and bronchogenic seeding of the lung tissue surrounding the infiltrate; 2) detection of Mycobacterium tuberculosis in sputum; 3) more frequent absence of leukocytosis and neutrophilic shift to the left in peripheral blood; 4) the lack of effect of treatment in the "set" terms for pneumonia. However, the latter provision can be used only with the correct determination of the etiology of lobar pneumonia and the appointment of adequate treatment.

Caseous pneumonia, one of the most severe forms of pulmonary tuberculosis, the frequency of which has increased dramatically in recent years, has more significant differences with lobar, in particular lobar, pneumonia. In contrast to lobar pneumonia, there is pronounced and constant sweating in caseous pneumonia, especially at night (with lobar pneumonia, sweating appears during a crisis or when the disease is complicated by abscess formation), usually not observed severe pain in the chest; already a few days after the onset of the disease, a large amount of greenish (purulent) sputum begins to separate (with croupous pneumonia, after a short period of rusty sputum, mucous sputum is determined in a small amount); hectic fever is noted (does not happen with croupous pneumonia); during auscultation, usually by the end of the 1st week of the disease, moist rales of increased sonority are determined. Of decisive importance for the diagnosis are the data of X-ray examination of the lungs and sputum analysis for Mycobacterium tuberculosis. Caseous pneumonia radiographically from the first days of the disease is characterized by inhomogeneous darkening of the lobe of the lung (less often 1-2 segments), which consists of merging large, flaky foci or infiltrative foci with emerging areas of enlightenment due to rapidly advancing decay. Within a few days, numerous fresh caverns with bay-shaped outlines are formed at the site of these areas. A rapid transition of the process to the adjacent lobe or to another lung is characteristic, with seeding of these departments and further development over several days of new confluent foci with their subsequent disintegration.

With inflammatory infiltrates of a non-lobar character, a differential diagnosis is often made between focal pneumonia and infiltrative pulmonary tuberculosis, but allergic lesions of the lungs must also be excluded. Tuberculous infiltrates are divided into several types: broncholobular, rounded, cloudy and periscissuritis, which refers to tuberculous infiltrate, located along a large or small interlobar fissure.

In contrast to focal pneumonia, infiltrative tuberculosis is observed:

    a more gradual and less noticeable onset of the disease, which is especially often observed with a rounded infiltrate;

    the absence or slight severity of the syndrome of intoxication and catarrhal phenomena. In particular, the cough in patients is not pronounced and has the character of "coughing". Often with infiltrative tuberculosis, the first clinical syndrome is hemoptysis, which appears as a "thunder from a clear sky" and already indicates the collapse of the infiltrate;

    most frequent localization in the upper lobe or in the VI segment (focal pneumonia is more often localized in the basal segments of the lower lobes);

    frequent detection of pallor of the face, profuse sweating at night, good tolerance elevated temperature body (the patient often does not feel its increase), poor percussion and auscultatory data (single wheezing is heard more often, usually after coughing). G. R. Rubinshtein's remark (1949) that in tuberculosis (more precisely, in its infiltrative form) "a lot is seen (meaning in an X-ray examination) and little is heard" remains relevant to this day;

    usually a normal or slightly elevated white blood cell count with a tendency to lymphocytosis. However, even with focal pneumonia, leukocytosis is absent in almost half of the patients. Therefore, only the detection of leukocytosis above 12 10 9 /l with a pronounced shift of the leukocyte formula to the left and ESR above 40 mm/h may indicate pneumonia;

    indications of contact with a patient with tuberculosis.

X-ray examination, detection of Mycobacterium tuberculosis in sputum, and in some cases bronchoscopy are of decisive importance for differential diagnosis.

Radiological differences are reduced to the following. With infiltrative tuberculosis, the shape of the darkening is round, less often cloudy or oblong at the interlobar fissure (with periscissuritis), the contours are often clear, the intensity is pronounced. Focal pneumonia is characterized by darkening of irregular shape with blurry contours, of low intensity. The main difference is the presence of soft (fresh) or dense focal shadows and a path to the root (due to lymphangitis and fibrosis) against the background of tuberculous infiltrate and next to it. With pneumonia, an expanded and infiltrated root is determined on the side of the lesion. Of some importance for diagnosis is the assessment of the dynamics of infiltration under the influence of nonspecific antibiotic therapy.

Allergic lesions of the lungs, with which it is necessary to differentiate pneumonia and infiltrative tuberculosis, occur in the form of: 1) eosinophilic pulmonary infiltrate (ELI), also called volatile ELI, simple pulmonary eosinophilia or Leffler's syndrome (described by Leffler in 1932); 2) prolonged pulmonary eosinophilia; 3) allergic pneumonitis; 4) allergic alveolitis. The need to exclude allergic processes in the lungs is dictated by the objectives of treatment, since the prescription and especially persistent use of antibiotics in allergic processes not only has no effect, but leads to a deterioration in the condition and often to death.

The greatest difficulty is the differential diagnosis with allergic pneumonitis, which often serve as manifestations of a drug disease, although they can also develop when exposed to other allergens. Allergic pneumonitis is a localized process in the lungs, often unilateral, which, according to clinical and radiological data, cannot be distinguished from pneumonia. Often the pleura is affected with the possible development of effusion. The idea of ​​​​the allergic nature of the pulmonary process is suggested by: 1) the development of the process against the background of taking medications (often penicillin drugs, sulfonamides, cephalosporins, furazolidone, adelfan, dopegit, vitamin B 1, cocarboxylase and many others); 2) an increase in the number of eosinophils in the peripheral blood in some patients and the presence of clinical manifestations of allergies (skin rashes, asthmatic bronchitis, conjunctivitis, etc.), however, in a significant percentage of cases, these signs are absent, since the possibility of an autonomous reaction of the lungs as an immunocompetent organ is allowed; 3) ineffectiveness of antibiotic therapy; 4) improvement after elimination of contact with the suspected allergen, for example, after the withdrawal of the "guilty" drug; 5) the effectiveness of glucocorticosteroids.

Allergic pneumonitis often overlaps with normal pneumonia. In these cases, at the beginning of the disease, antibiotics give a certain effect, but then the reverse development of the process stops, despite the change of antibiotics (antibiotic); moreover, the process spreads to neighboring parts of the lungs, and sometimes destructive changes develop and hemoptysis appears, which is explained by hemorrhagic vasculitis and impaired microcirculation. Pulmonary destruction in allergic pneumonitis develops due to aseptic necrosis and, unlike abscessing pneumonia, its formation is not preceded by the separation of purulent sputum, and the cavity itself initially does not contain fluid. In the future, its secondary infection often occurs with the formation of an abscess.

If the patient has pneumonia, then they proceed to the fourth stage - differential diagnosis between various forms of pneumonia according to the etiological factor.