Eosinophilic infiltrate in the lungs. Pulmonary eosinophilic infiltrate. What diseases occurs

Eosinophilic pneumonia. Eosinophilic infiltrate in the lungs (Leffler's syndrome).

Treatment. If helminths are found, deworming is carried out. If the symptoms of the infiltrate itself persist for more than long time or pronounced, the use of corticosteroids (prednisolone up to 20-30 mg / day) in the form of a short course is justified.

LESSON #5

DIFFERENTIAL DIAGNOSIS OF NON-INFLAMMATORY LUNG INFILTRATS

Tuberculous infiltrate represents a bronchopneumonic inflammatory focus in the lung. In the center of it, caseosis characteristic of tuberculous inflammation is determined. Caseous necrosis can be mild, sometimes leading to the formation of a cavity.

Infiltrative tuberculosis can occur both as a result of the activation of old tuberculous changes, and as a result of the progression of a fresh focal process. In this case, the infiltrate is preceded by fresh focal tuberculosis. Infiltrative pulmonary tuberculosis can occur as a result of lymphobronchogenic spread of mycobacteria from caseous-altered lymph nodes of the mediastinum. Quite often at such patients the endobronchitis is also noted. The infiltrative process is often localized in the middle and lower parts of the lungs.

By the nature of the radiological data and partly due to the peculiarities of the clinical picture and the course of the disease, several clinical and radiological variants of infiltrative tuberculosis are distinguished:

Cloudy, characterized by the presence of a gentle low-intensity homogeneous shadow with fuzzy, blurry contours;

Round (type Assman) - round shape homogeneous shadow of low intensity with clear contours;

Lobit is an extensive infiltrative process that captures the whole lung lobe, the shadow is most often inhomogeneous in nature, often with the presence of single or multiple decay cavities;

Periscissuritis is an extensive infiltrative shadow with, on the one hand, a clear edge, on the other, a blurry one. This character of the shadow is determined by the defeat of one or two segments located along the interlobar fissure. Often there is also a lesion of the interlobar pleura, sometimes with accumulation of effusion;

Lobular - an inhomogeneous shadow, which is large and small foci, merged into one or more conglomerates, in the center of which decay is often detected.

For all clinical and radiological options, not only the presence of an infiltrative shadow, often with decay, is characteristic, but bronchogenic seeding is also possible. Often, patients with infiltrative tuberculosis have various types of endobronchitis. If the patient has an extremely severe course of infiltrative tuberculosis, which is characteristic of infiltrative-caseous and caseous pneumonia, this should be reflected in the diagnosis. In the first days, with the rapid liquefaction of the formed caseous masses, a giant cavity or multiple small cavities are formed, in which case the diagnosis is confirmed both by the dynamics of the process and by the appearance of abundant bacterial excretion.

In most patients with infiltrative tuberculosis, the clinical picture of the disease is characterized by an increase in body temperature; the temperature may not last long (6-5 days). There is an increase in temperature to 38-38.5 ° C, as well as other symptoms of intoxication. Patients may develop sweating, work capacity decreases, a cough appears, which is not painful and does not always attract the attention of the patient, as in focal pulmonary tuberculosis, but for the most part accompanied by mucus.

Sometimes infiltrative pulmonary tuberculosis is accompanied by hemoptysis - this is a symptom that occurs more often than with focal tuberculosis. When listening to patients with infiltrative tuberculosis, especially in the presence of decay, wheezing is determined. After the start of treatment, wheezing quickly disappears. With extensive infiltrates, there may be dullness in the corresponding areas of the lungs, altered breathing, but these manifestations of infiltrative tuberculosis are not as pronounced as with banal pneumonia.

An important diagnostic method is bacteriological diagnosis. Mycobacterium tuberculosis can be detected both by microscopy and by culture. One of the important signs of infiltrative tuberculosis is a characteristic blood picture. In patients with infiltrative pulmonary tuberculosis, as a rule, there is no high leukocytosis with increase in ESR, while in patients with pneumonia, leukocytosis, shift to the left are typical signs.

Bronchoscopy is important method diagnostics, although not always with infiltrative pulmonary tuberculosis, concomitant specific endobronchitis is noted.

Two main variants of the course of infiltrative pulmonary tuberculosis can be distinguished:

Progressive course, characterized by the rapid formation of destruction. At the same time, the dissociation between the clinical manifestations of the disease and the dynamics of morphological changes in the lungs attracts attention. Elevated body temperature, characteristic of the onset of infiltrative tuberculosis, gradually decreases 10-15 days after the onset of the disease. By this time, the severity of "chest" symptoms decreases or they disappear altogether (cough, sputum production, disappearance of previously determined wheezing). In the absence of treatment, after a while, the "chest" symptoms and intoxication resume in patients, i.e., an exacerbation develops. All this undulating process is accompanied by the formation of a cavity and ongoing bacterial excretion;

An involutive course that takes place under conditions of rational treatment. It is characterized by the gradual disappearance of the clinical manifestations of the disease and earlier - "chest" symptoms, and then symptoms of intoxication, a subjective feeling of restoration of health, as a rule, during the first 3 months - the cessation of excretion of Mycobacterium tuberculosis with sputum. Morphological changes in the lungs undergo involution more slowly, they are characterized by the resorption of inflammatory changes and the closure of the cavity, if it has had time to form.

Eosinophilic lung infiltrate

(synonymous with eosinophilic pneumonia) is a form of Loeffler's syndrome. It is characterized by the detection of an infiltrative shadow on the radiograph of the lung, blood eosinophilia, the rapid disappearance of all symptoms and the complete resorption of infiltrates, the absence or scarcity of painful disorders. It is impossible to judge the true frequency of the disease; it seems to occur frequently. Eosinophilic infiltrate is an allergic disease. Among the agents that cause it are various medicines, vaccines, helminthic, microbial and plant allergens. The infiltrate is usually discovered incidentally. Some patients complain of feeling unwell, subfebrile temperature, cough, separation of mucous or mucopurulent sputum, which may have a canary color, metallic taste and contain blood. Occasionally, shortening of the percussion sound, scanty moist rales and pleural friction noise are heard above the infiltrates. The x-ray picture is varied and often atypical (see Art. 57). The main feature of peripheral blood is eosinophilia, sometimes accompanied by leukocytosis. It usually grows more slowly than radiological changes, reaching a maximum on the 3-7th day of illness or later. Eosinophils and Charcot-Leiden crystals are sometimes found in sputum. The thought of an eosinophilic infiltrate should arise if pronounced and, apparently, fresh radiographic changes in the lungs are accompanied by eosinophilia. The diagnosis is confirmed if, after a few days, the shadows found disappear. It is reinforced by the presence of other allergic diseases in the patient in the past or present, the absence of causative agents of tuberculosis in sputum, and sometimes negative results of tuberculin tests. It is more difficult to diagnose with severe or prolonged eosinophilic infiltrate and its combination with other lung diseases. The prognosis is favorable, although relapses are possible. Treatment consists in a sparing regimen and, if possible, in the elimination of the active allergen.

Pulmonary embolism(PE) - blockage of the pulmonary artery or its branches by blood clots, which are formed more often in large veins lower extremities or pelvis (embolism). In foreign literature, a broader concept is common pulmonary embolism, which also includes rare air, fat, amniotic fluid, foreign bodies, tumor cells.

Causes and risk factors

The disease is based on thrombosis, which is facilitated by three factors (Virchow's triad): impaired blood flow, damage to the endothelium of the vascular wall, hypercoagulation, and inhibition of fibrinolysis.

Violation of blood flow is caused by varicose veins, compression of vessels from the outside (tumor, cyst, bone fragments, enlarged uterus), destruction of vein valves after phlebothrombosis, as well as immobilization, which disrupts the function of the musculo-venous pump of the lower extremities. Polycythemia, erythrocytosis, dehydration, dysproteinemia, elevated fibrinogen increase blood viscosity, which slows down blood flow.

When the endothelium is damaged, the subendothelial zone is exposed, which triggers a cascade of blood coagulation reactions. The reasons for this are direct damage to the vessel wall during the installation of intravascular catheters, filters, stents, vein prosthetics, trauma, and surgery. Hypoxia, viruses, endotoxins also lead to damage to the endothelium. With a systemic inflammatory reaction, leukocytes are activated, which, when attached to the endothelium, damage it.

The source of blood clots in PE is more often the veins of the lower extremities (thrombosis of the veins of the lower extremities), much less often - the veins of the upper extremities and the right heart. In pregnant women, as well as in women who have taken oral contraceptives for a long time.

Pathogenesis

Embolization is caused by thrombi freely located in the lumen of the vein, attached to its wall only in the zone of its base (floating thrombi). A detached blood clot with blood flow through the right parts of the heart enters the pulmonary artery, obliterating its lumen. The consequences of this depend on the size, number of emboli, the reaction of the lungs and the activity of the thrombolytic system of the body.

Thromboembolism

With small emboli, there are no symptoms. Large emboli worsen the perfusion of segments or even entire lobes of the lung, which leads to disruption of gas exchange and the development of hypoxia. In response to this, the lumen of the vessels of the pulmonary circulation narrows reflexively, and the pressure in the pulmonary arteries increases. The right ventricular load increases due to high pulmonary vascular resistance caused by obstruction and vasoconstriction. With thromboembolism of small branches of the pulmonary artery, it is not accompanied by hemodynamic disorders and in 10% of cases pulmonary infarction and secondary infarct pneumonia develop.

Classification

Clinically, PE is classified into the following types:

massive - more than 50% of the volume of the vascular bed of the lungs is affected (embolism of the pulmonary trunk and / or main pulmonary arteries) and the disease presents with shock and/or systemic hypotension;

submassive - 30 - 50% of the volume of the vascular bed of the lungs is affected (embolism of several lobar or many segmental pulmonary arteries) and is manifested by symptoms of right ventricular failure;

non-massive - less than 30% of the volume of the vascular bed of the lungs is affected (embolism of small distal pulmonary arteries), manifestations are absent or minimal (pulmonary infarction).

Clinical picture

Often, PE is asymptomatic. But the emerging clinical manifestations are nonspecific, which makes diagnosis difficult.

Massive PE is manifested by acute right ventricular failure with the development of shock and systemic hypotension (lowering blood pressure<90 мм рт.ст. или его падение на ≥40 мм рт.ст., что не связано с аритмией, гиповолемией или сепсисом). Могут возникать одышка, тахикардия, обморок. При субмассивной ТЭЛА артериальная гипотензия отсутствует, а давление в малом круге кровообращения повышается умеренно. При этом обнаруживают признаки дисфункции правого желудочка сердца и/или повреждения миокарда, что свидетельствует о повышенном давлении в лёгочной артерии. При немассивной ТЭЛА симптомы отсутствуют и через несколько дней возникает инфаркт лёгкого, который проявляется болью в грудной клетке при дыхании (за счёт раздражения плевры), лихорадкой, кашлем и, иногда, кровохарканьем и выявляется рентгенологически (типичные треугольные тени).

Auscultation of the heart reveals amplification and accent of the II tone over the tricuspid valve and pulmonary artery, systolic murmur at these points. Possible splitting of the II tone, gallop rhythm, which is considered a bad prognostic sign. In the area of ​​lung infarction, weakening of breathing, wet rales and pleural friction noise are heard.

Diagnostics

Diagnosis is difficult because the symptoms of PE are nonspecific and diagnostic tests are imperfect. Standard examination methods (routine laboratory tests, electrocardiography (ECG), chest x-ray) are useful only to rule out other pathologies (eg, pneumonia, pneumothorax, rib fractures, myocardial infarction, pulmonary edema). Sensitive and specific methods for diagnosing PE include the determination of d-dimer, echocardiography, computed tomography (CT), ventilation-perfusion scintigraphy, pulmonary angiography, as well as methods for diagnosing deep vein thrombosis of the lower extremities (ultrasonography, CT venography).

Determination of the level of d-dimers

D-dimer - fibrin breakdown product; its elevated level suggests recent thrombus formation. Determination of the level of d-dimers is a highly sensitive (more than 90%), but not specific method for diagnosing PE. This means that an increase in the level of d-dimers occurs in a large number of other pathological conditions (eg, infection, inflammation, necrosis, aortic dissection). However, the normal level of d-dimers (<500 мкг/л) позволяет исключить ТЭЛА у пациентов с низкой и средней вероятностью.

Electrocardiography

On the ECG of a patient with PE, sinus tachycardia (approximately 150 beats per minute) and right bundle branch block.

Signs of PE on the electrocardiogram are not specific and are absent in most patients. Sinus tachycardia, high and pointed P wave (P-pulmonale, a sign of right atrial overload) are often detected. Approximately 20% of patients may show signs of acute cor pulmonale (right ventricular overload): deviation of the electrical axis of the heart to the right; syndrome S I Q III T III (McGinn-White syndrome) - a deep S wave in lead I, a pronounced Q wave and a negative T wave in lead III; new blockade of the right leg of the bundle of His; deep S waves in V 5-6 combined with negative T waves in V 1-4. However, acute cor pulmonale can also occur in other acute pathologies of the respiratory system (massive pneumonia, a severe attack of bronchial asthma).

Chest X-ray

Chest x-ray reveals signs of pulmonary hypertension of thromboembolic origin: high standing of the dome of the diaphragm on the side of the lesion, expansion of the right heart and roots of the lung, Pall's sign (dilation of the right descending pulmonary artery), Westermarck's symptom (English) Russian. (local depletion of the vascular pattern of the lung), discoid atelectasis. With lung infarction - Hampton's triangle (English) Russian. (seal cone-shaped with the apex facing the gates of the lungs), pleural effusion on the side of the lesion.

Ultrasound examination of deep veins of the lower limb

Ultrasound examination (ultrasound) of peripheral veins can detect blood clots in the veins of the lower extremities. In most cases, they serve as a source of thromboembolism. For this, two methods are used. The first is compression ultrasound; while in the B-mode receive a cross section of the lumen of the arteries and veins. Then the ultrasonic sensor is pressed on the skin in the projection of the vessels. If there is a thrombus in the vein, its lumen does not decrease (compression does not occur). Another technique is Doppler ultrasound; at the same time, using the Doppler effect, the velocity of blood flow in the vessels is determined. Decreased blood flow in the veins is a possible sign of blockage by a blood clot. The combination of compression and Doppler ultrasound is called duplex ultrasonography.

To fungal infections of the lungs include candidiasis, aspergillosis, coccidioidomycosis, histoplasmosis, blastomycosis, paracoccidioidomycosis, sporotrichosis, cryptococcosis, mucormycosis, and a few other lesions.

Candidiasis of the lungs

Pathogen: yeast-like fungus of the genus Candida. The most important are Candida albicans, Candida tropicans. Candidiasis is widespread, but more common in the tropics. The main source of infection is a patient with acute forms of candidiasis of the skin and mucous membranes. Infection occurs through direct contact with an infected person and when using common household items (bath, linen, etc.).

Pathogenesis

Fungi of the genus Candida are commonly found in the mouth, stool, and vagina. Local factors, as well as factors that depend on the state of the body, lead to the penetration of fungi into tissues through damaged skin and mucous membranes, with perforation of the gastrointestinal tract as a result of trauma or surgery, with prolonged use of catheters and burns. Patients with diabetes, HIV infection, oncohematological diseases, pregnant women, on the background of antibiotic or glucocorticoid therapy are in a potentially threatened position. Candidiasis is a common complication of neutropenia, thus confirming the important role of neutrophils in protecting the body from infection. Lung damage can occur in the form of primary and secondary, acute and chronic candidiasis. The primary usually proceeds in an acute form, the secondary - in a chronic one. Primary acute pulmonary candidiasis usually develops during treatment with antibiotics, glucocorticosteroids, cytostatics and antimetabolites.

Clinical picture

The severity of the disease can be mild, moderate, severe. Characterized by weakness, malaise, decreased performance, headache. Body temperature usually remains normal. In some patients, the disease begins acutely with a rise in temperature to high numbers. There is a "scratching" dry cough, chest pain associated with breathing. With a mild course in the initial stage, the disease resembles bronchitis with a strong cough without sputum or with scanty, grayish sputum, sometimes with the smell of yeast, with dry and moist coarse and medium bubbling rales. In a more severe course and at a later date, focal or lobar pneumonia, characteristic unstable volatile infiltrates, may appear. In severe cases, candidal pneumonia can be complicated by pleurisy. The general condition is usually severe, high or moderate fever, almost constant cough, accompanied by copious sputum, hemoptysis, often dull pain in the chest.

Diagnostics

Hemogram changes are uncharacteristic. Leukopenia, basophilia, eosinophilia, neutrophilia, monocytosis, and lymphopenia are possible. X-ray picture. The radiograph reveals multiple patchy shading due to small pneumonic foci and atelectasis. Larger lesions are usually located in the lower parts of the lungs. Sometimes there are miliary shading ("snow flakes"). The roots of the lung are expanded. Sometimes heavy shadows are found from the foci of shading, going to the hilar lymph nodes. The cavernous form is characterized by the appearance of thin-walled cavities and their relatively rapid regression up to complete disappearance under the influence of antifungal treatment. Specific Diagnosis is based on the isolation of the pathogen from sputum, bronchial secretions and respiratory lavage. Complement fixation reaction, agglutination reaction is used. The method of fluorescent antibodies is highly sensitive. An intradermal test with a candidal allergen is used.

Treatment

For skin candidiasis, local treatment is carried out with nystatin powder or cream containing ciclopirox. Candidiasis of the oral mucosa responds better to clotrimazole tablets (5 times a day) than to a suspension with nystatin. Ketoconazole 200–400 mg/day or fluconazole 100–200 mg/day are effective in esophageal candidiasis. In severe cases, amphotericin B 0.3 mg/kg per day is used intravenously for 5-10 days. In HIV infection, fluconazole is considered the most effective drug in the treatment of candidiasis of the oral cavity and esophagus. In case of bladder candidiasis with a catheter in it, irrigation is carried out with a solution of amphotericin B at a dose of 50 mg/l; patients with candiduria are given oral fluconazole. In the disseminated form, amphotericin B at a dose of 0.4–0.5 mg/kg per day or at a double dose every other day is the drug of choice. Flucytosine 100-150 mg/kg per day is added to the treatment, reducing the dose of amphotericin B to 0.3 mg/kg per day, if there are no contraindications to the drug. Fluconazole at a dose of 400 mg per day is used for prophylaxis in patients with immunodeficiency. It can be used to complete the treatment of patients with liver candidiasis, if they do not have neutropenia. Candida krusei is resistant to fluconazole.

Aspergillosis of the lungs

The causative agents are moldy fungi of the genus Aspergillus. Aspergillus fumigatus is of clinical importance.

Pathogenesis

The disease is caused by inhalation of spores of the fungus with subsequent penetration into the lungs in immunocompromised patients. 90% of patients at risk of infection have 2 or 3 factors: less than 500 granulocytes, high-dose glucocorticoids, or treatment with cytostatics (azathioprine). An invasive variant of aspergillosis can occur with HIV infection, usually with T-helper depletion and neutropenia. Characterized by the spread of blood vessels, the occurrence of tissue necrosis, hemorrhagic infiltrates. Aspergillus can also spread through the damaged bronchial tree, colonizing cysts that have not yet been infected in the lungs or cavities. It often occurs as a secondary disease in debilitated, malnourished patients, especially against the background of diabetes mellitus, tuberculosis, blood diseases, and immunodeficiency states. The occurrence is also promoted by long-term therapy with antibiotics, corticosteroids, immunosuppressants. In most cases, aspergilloma occurs in sanitized tuberculous caverns, cavities after abscesses, bronchiectasis and is a tangle of fungal filaments. Localized in the upper parts of the lungs, often on the right.

Clinic

Characterized by an increase in weakness, anorexia, fever, chills and significant sweating often occur. The main symptom is a strong paroxysmal cough with the release of copious blood-colored sputum containing greenish flakes (accumulations of mycelium of the fungus) and streaks of blood. Sometimes there is hemoptysis. Sometimes the disease is accompanied by attacks of suffocation. This form of the disease often occurs in people with a burdened allergic history, working in flour mills, weaving, grain warehouses and poultry farms, in greenhouses. Attacks of suffocation are often combined with allergic alveolitis, fever and infiltration of the lung tissue. In the later stages of the disease, pneumofibrosis, bronchiectasis, and cor pulmonale develop.

Diagnostics

In the sputum, drusen and aspergillus mycelium are isolated. Re-isolation of Aspergillus from sputum is indicative of colonization or infection. In the blood - leukocytosis, eosinophilia, elevated ESR. On a chest x-ray, small foci are found, partially compacted, sometimes calcified, against the background of pneumosclerosis and compaction of the roots of the lungs. In some cases, the foci have the character of spherical formations resembling tuberculoma. Diagnosis requires a biopsy that proves tissue damage and a positive culture result. Blood cultures are rarely positive. Serum IgG antibodies to Aspergillus can be detected in colonized patients and in almost all patients with fungal filament balls.

Complications

Lung abscess. The course of the disease is severe, high fever, shortness of breath, chest pain, hemoptysis. An increase in weakness, anorexia, an increase in body temperature are characteristic, chills and significant sweating often occur. The main symptom is a strong paroxysmal cough with the release of copious blood-colored sputum containing greenish flakes (accumulations of mycelium of the fungus) and streaks of blood. In the absence of drainage through the bronchus, this symptom is absent. Physically - signs of a cavity or infiltrative process in the lung. Pleurisy. In patients with pulmonary tuberculosis treated in the past with artificial pneumothorax, after pneumonectomy or lobectomy, performed for tuberculosis or lung cancer and accompanied by the formation of a bronchopleural fistula, in patients with reduced immunity, as well as with systemic aspergillosis, pleurisy may develop. In the pleural fluid, which has the character of an exudate, brown lumps containing mushrooms are found. Pleural fluid culture for fungal infection is positive. Positive precipitation reaction in the study of exudate with a specific antiserum. Calcium oxalate crystals are found in the pleural fluid.

- this is an allergic-inflammatory lesion of the lung tissue, accompanied by the formation of unstable migrating infiltrates of an eosinophilic nature and the development of hypereosinophilia. The disease usually occurs with malaise, subfebrile condition, a small dry cough, sometimes with scanty sputum; in the acute form - with chest pain, myalgia, the development of acute respiratory failure. To establish eosinophilic pneumonia, X-ray data and CT scan of the lungs, a complete blood count, bronchoalveolar lavage, allergy tests, and serodiagnosis allow. The basis of treatment is specific desensitization and hormonal therapy.

ICD-10

J82 Pulmonary eosinophilia, not elsewhere classified

General information

The reasons

Eosinophilic pneumonia may be the result of an allergic reaction to medication (penicillin, acetylsalicylic acid, sulfonamides, nitrofurans, isoniazid, hormonal and radiopaque drugs, gold compounds), to contact with chemical agents at work (nickel salts). Atopic sensitization of the respiratory tract to fungal spores (especially Aspergillus), pollen (lily of the valley, lily, linden) also contributes to the development of eosinophilic pulmonary infiltrates. Eosinophilic pneumonia may be a manifestation of serum sickness and may be associated with tuberculin allergy.

Pathogenesis

The development of eosinophilic pneumonia is mediated by immediate-type hypersensitivity reactions. In addition to hypereosinophilia in the blood of patients, an elevated level of IgE (hyperimmunoglobulinemia) is often detected. Mast cells activated by immune (IgE) and non-immune (histamine, complement system) mechanisms and producing allergy mediators (mainly eosinophilic chemotactic factor of anaphylaxis) are responsible for the formation of allergic-inflammatory foci in the lung tissue. In some cases, eosinophilic pneumonia develops due to the production of precipitating antibodies to antigens (reactions like the Arthus phenomenon).

Symptoms of eosinophilic pneumonia

The clinical picture is highly variable. Allergic pneumonia can have an asymptomatic course with no or very poor severity of complaints and can be determined only by X-ray and clinical and laboratory methods. Often, Loeffler's pneumonia occurs with minimal manifestations, manifesting symptoms of catarrhal rhinopharyngitis. Patients feel a slight malaise, weakness, fever to subfebrile, a small cough, often dry, sometimes with slight viscous or bloody sputum, pain in the trachea. With a massive hematogenous spread of eggs and larvae of worms in the body, a skin rash, itching, shortness of breath with an asthmatic component join. Eosinophilic infiltration of other organs is accompanied by mild, quickly disappearing signs of their defeat - hepatomegaly, symptoms of gastritis, pancreatitis, encephalitis, mono- and polyneuropathy.

Acute eosinophilic pneumonia is severe, with intoxication, febrile condition, chest pain, myalgia, rapid (within 1-5 days) development of acute respiratory failure, respiratory distress syndrome. For the chronic form, a subacute course is typical with sweating, weight loss, increased dyspnea, and the development of pleural effusion.

Eosinophilic pneumonia usually lasts from a few days to 2-4 weeks. Recovery may occur spontaneously. In the chronic form, the prolonged existence of infiltrates and relapses contribute to the gradual progression of the disease, the development of pulmonary fibrosis and respiratory failure.

Diagnostics

Diagnosis of eosinophilic pneumonia includes x-rays and CT scans of the lungs, complete blood count, fecal analysis for worm eggs, bronchoalveolar lavage, allergy tests, serological (RP, RSK, ELISA) and cellular tests (degranulation reactions of basophils and mast cells). Patients with eosinophilic pneumonia usually have a previous allergic history. Auscultation reveals a small amount of moist fine bubbling rales or crepitus. With extensive infiltrates, a shortening of the pulmonary sound during percussion is noticeable.

In the acute form of eosinophilic pneumonia, glucocorticoids are used, against which a rapid (within 48 hours) regression of inflammation occurs. The dose of HA is selected individually and reduced gradually to avoid exacerbation. In severe cases, mechanical ventilation, long-term hormonal therapy are required. With bronchial obstruction, inhaled GCs, beta-agonists are indicated. For better sputum discharge, expectorants and breathing exercises are used. Treatment of concomitant bronchial asthma.

Forecast and prevention

The prognosis of eosinophilic pneumonia is generally favorable, spontaneous resolution of infiltrates is possible. Proper treatment and observation by a pulmonologist allows you to avoid chronicity of the process and relapses. Prevention of eosinophilic pneumonia is reduced to hygiene measures that prevent infection of the body with helminths, control over medication intake, limiting contact with aeroallergens, and specific hyposensitization. If necessary, it is recommended to change jobs.

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The worst Best

Pathological changes include foci of infiltration, which, on microscopic examination, are exudation into the alveoli with a large number of eosinophils. In some cases, perivascular infiltration with leukocytes and small thromboses are observed.

clinical picture. In most patients, pulmonary eosinophilic infiltrate with ascariasis and other helminthic invasions is asymptomatic and is detected during preventive fluorographic studies. Body temperature is usually normal, sometimes it rises to subfebrile figures with normalization within a few days. In some patients, the appearance of a pulmonary eosinophilic infiltrate is accompanied by malaise, headache, night sweats, cough without sputum or with a small amount of yellow sputum. A slight shortening of the percussion tone and moist rales over the site of the infiltrate may be detected. All symptoms quickly, within 1-2 weeks, disappear.

Radiologically, non-intense, homogeneous shading is determined in various parts of the lungs without clear boundaries. Shadows may be localized in both or one lung, may disappear in one place and appear in others. More often the shadows are small in size, but sometimes they can spread to almost the entire lung. Shading usually disappears after 6-12 days.

It is necessary to re-examine the faeces for the presence of helminth eggs. In cases of fresh invasion, the migration of ascaris larvae and pulmonary eosinophilic infiltrates occur before the appearance of ascaris and their eggs in the feces.

A characteristic feature is eosinophilia.

Differential Diagnosis carried out with tuberculosis, pneumonia and pulmonary infarction. Distinctive features of pulmonary eosinophilic infiltrate are the ease of the course of the disease, "volatility" and the rapid disappearance of pulmonary infiltrates, peripheral blood eosinophilia.

Treatment consists of deworming. Any treatment directed directly at the pulmonary infiltrate is usually not required. If the manifestations of the disease are pronounced or persist for a long time, treatment with corticosteroid hormones can be carried out.

A special place among pulmonary eosinophilic infiltrates is occupied by tropical pulmonary eosinophilia, which occurs in India, Burma, Malaysia and Ceylon and is associated with invasion by filariae.

The clinical picture is characterized by a latent onset, the appearance of a dry or with a small amount of sputum, a mucous cough, which is sometimes paroxysmal in nature and is especially pronounced at night. Some patients develop wheezing when they cough. Lung auscultation reveals scattered dry rales.

Severe eosinophilia, the presence of eosinophils in the sputum, and a positive complement fixation reaction with the filarial antigen are characteristic. Filariae can be detected on a lymph node biopsy.

Treatment is with antifilarial drugs. In some patients, spontaneous recovery is possible, however, in patients who have not received special treatment, the disease can proceed for a long time - months and years, with repeated exacerbations, leading to the development of pneumosclerosis.

Pulmonary eosinophilic infiltrates can occur from exposure to many drugs and chemical compounds: furadonin, acetylsalicylic acid, azathioprine, chlorpropamide, chromoglycate, isoniazid, methotrexate, penicillin, streptomycin, sulfonamides, beryllium, salts of gold and nickel, etc. In addition, eosinophilic pulmonary infiltrates can appear after inhalation of the pollen of some plants, house dust, animal dander.

In acute reactions to chemical agents, no special treatment is required, and the cessation of the action of the factor that caused the pulmonary infiltrate leads to the complete disappearance of the signs of the disease. In some cases, with a protracted course of the disease, corticosteroids are required.

Pulmonary eosinophilic infiltrates in patients with bronchial asthma in half of the cases are associated with exposure to the patient Aspergillus fumigatus.

The clinical picture in a significant proportion of patients is characterized by a severe course of bronchial asthma. Exacerbation of the disease is accompanied by an increase in body temperature, sometimes to high numbers. A cough is characteristic, which is paroxysmal and is accompanied by the discharge of thick sputum in the form of plugs and casts of the bronchi.

Pulmonary eosinophilic infiltrates are found in periarteritis nodosa and its variant, Wegener's granulomatosis.

Lung infiltration is a clinical syndrome in which the normal airiness of the lung tissue is replaced by a pathological substrate of increased density, most often of an inflammatory nature. At the same time, an area is formed in the parenchyma of the lungs, characterized by an increased volume and increased density, as well as an accumulation of cellular elements unusual for it.

The reasons

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

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

The classic course of the syndrome of infiltration in the lungs is observed in pneumonia and involves a successive change of three phases of the inflammatory process:

• alteration under the influence of damaging factors and the 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 voice trembling, determined by palpation;
• weakened vesicular or bronchial breathing on 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, and pain in the chest (with involvement of the pleura in the pathological process).

Differential diagnosis of pulmonary infiltrates

Identification of signs of infiltration of the lung tissue leads the doctor to a diagnostic search. At the same time, the patient's complaints, the history of the disease, 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. Such a course is characteristic of pneumosclerosis or a tumor process.
• In the presence of fever, it can be pneumonia, lung abscess in the stage of infiltration, pulmonary infarction, festering cyst, etc.

If any of these diseases is suspected, the specialist will refer the patient to. This study allows not only to confirm the presence of infiltration by identifying the “blackout” area on the radiograph, but also to assess its size, shape and intensity.

If patients with infiltration syndrome do not complain about their health and they have this pathology during a routine x-ray examination, then the reasons for it 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;
• CT scan.

Diseases that occur with the syndrome of infiltration of the lung tissue have their own characteristics, we will consider some of them.

Syndrome of lung infiltration in croupous pneumonia

The disease begins acutely and goes through 3 stages in its course. On his example, one can trace the classic course of the lung 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 concerned about dry cough, fever, mixed shortness of breath, weakness. Objectively, signs of infiltration of the lung tissue are detected (decrease in the elasticity of the lung tissue, dullness of percussion sound, weakened vesicular breathing, etc.). At the same time, side respiratory noises are heard in the form of crepitus "tide".
2. In the second stage of the disease, the alveoli are completely filled with exudate and the lung tissue approaches the density of the liver. The clinical picture changes: the cough becomes wet with a rusty sputum, chest pain appears, shortness of breath increases, body temperature remains high. Bronchial breathing is heard over the affected area. With percussion, a more pronounced dullness of the percussion sound is determined.
3. At the third stage, the inflammatory process is resolved, the exudate in the alveoli is absorbed, air begins to flow into them. The patient's body temperature decreases, shortness of breath decreases, productive cough with separation of mucopurulent sputum is disturbing. Weakened breathing, crepitation of the “low tide” and small bubbling moist rales are heard above the lungs.

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

Infiltrative form of tuberculosis

This pathology has an erased clinical picture, complaints may either be absent altogether, or limited to:

• weakness;
• sweating;
• low temperature;
• cough with sputum, in which the study reveals Mycobacterium tuberculosis.

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

Eosinophilic pulmonary infiltrate

The disease proceeds easily, physical symptoms are poor. Persons suffering from this pathology are concerned about weakness, an increase in body temperature to subfebrile numbers.

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

The reasons for this condition may be:

• helminthic invasion;
• taking antibiotics;
• administration of radiopaque agents.

Pneumonia in pulmonary infarction

Infiltration of the lungs in this disease is often preceded by a clinic of pulmonary embolism. These patients are concerned about:

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

Usually they have thrombophlebitis of the veins of the lower extremities.

Pneumonia with bronchial obstruction by a tumor

This disease can manifest itself long before the detection of an infiltrative process. It may be preceded by:

• prolonged subfebrile condition;
• 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 the poverty of objective signs. Sputum examination 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 a radiograph or detected during an objective examination in the form of: