Eosinophilic infiltrate in the lungs. Types of eosinophilic infiltrates. chronic pneumonia. What is an infiltrate

Description:

In most patients, pulmonary eosinophilic infiltrate associated with ascariasis and other helminthic invasions is asymptomatic and is detected during preventive fluorographic studies. Body temperature is usually normal, sometimes it rises to sub-febrile 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 stained in yellow sputum.

On physical examination, a slight shortening of the percussion tone and moist rales over the site of infiltration in the lungs can be detected. All of the above symptoms and physical signs disappear quickly, within 1-2 weeks.

Clinical manifestations occur on average 2 hours - 10 days after the start of administration. medicines and are characterized the following symptoms:
   dry ;
   chest pain;
  
   fever with chills;
   arterial hypotension;
  
   .

Causes of occurrence:

The pathogenesis of these changes is not well understood. There is an idea of ​​the leading role of sensitization and allergies arising from helminthic invasion. One of the proofs of this point of view is the increase in the content of IgE in the blood serum of patients.

Pathological anatomical changes consist in the appearance of foci of infiltration in the lungs, which, on microscopic examination, are alveolar exudation with a large number of eosinophils. In some cases, perivascular infiltration with leukocytes and small thromboses were observed.

Treatment:

Diegylcarbamazine is the most effective antifilarial drug. Some patients may spontaneously recover, but in patients who have not undergone 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 may occur from drug exposure and chemical compounds. Pulmonary eosinophilic infiltrates that develop under the influence of furadoin are described. acetylsalicylic acid, azathioprine, chlorpropamide, chromoglycate, isoniazid, metatrexate, penicillin, streptomycin, sulfonamides, beryllium, salts of gold and nickel and other compounds. In addition, eosinophilic pulmonary infiltrates may appear after pollen inhalation of some plants.

The clinical picture of the pulmonary eosinophilic infiltrate that occurs after the use of furadonin is described in particular detail. Lung reactions to furadonin are acute and chronic. In an acute variant of the reaction, fever, dry cough, runny nose, shortness of breath appeared 2 hours to 10 days after the start of furadonin intake. On radiographs, diffuse changes in the lungs are usually detected, sometimes focal irregularly shaped infiltrates in the lungs, there were no rapid disappearance and migration of infiltrates typical of Loeffler's syndrome, sometimes effusion appears, and the pleural fluid contains many eosinophils. An increased content of eosinophils in the blood is characteristic. In the acute course of the disease, the eosinophilic infiltrate in the lung disappears shortly after discontinuation of the drug. In the chronic course of the disease, the resorption of the pulmonary eosinophilic infiltrate is delayed, and in some cases pneumosclerosis develops in its place.

Treatment. Acute reactions medicines and chemical agents do not require special therapy, and the cessation of the action that caused the pulmonary infiltrate of the factor leads to the complete disappearance of the signs of the disease. In some cases, when protracted course disease requires the use of glucocorticosteroid drugs.

Pulmonary eosinophilic infiltrates in patients with bronchial asthma in half of the cases are associated with exposure to the patient Aspergillus fumigatus. In some cases, eosinophilic infiltrates are caused by inhalation of plant pollen, house dust, animals. The dryness of the air contributes to the occurrence of this condition, which causes drying of the mucous membrane of the respiratory organs, the formation of thick mucus in the bronchi and a violation of mucus secretion. Changes often occur in patients with bronchial asthma older than 40 years and predominantly in women.

At morphological study areas of the lungs are found filled with exudate containing a large number of eosinophils, which are also present in the lumen of the bronchi and sometimes infiltrate their walls.

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

The pathogenesis of these changes is not well understood. There is an idea of ​​the leading role of sensitization and allergies arising from helminthic invasion. One of the proofs of this point of view is the increase in the content of IgE in the blood serum of patients.

Pathological anatomical changes consist in the appearance of infiltration foci in the lungs, which, on microscopic examination, are alveolar exudation with a large number of eosinophils. In some cases, perivascular infiltration with leukocytes and small thromboses were observed.

Symptoms of Pulmonary eosinophilic infiltrate:

In most patients, pulmonary eosinophilic infiltrate associated with ascariasis and other helminthic invasions is asymptomatic and is detected during prophylactic fluorographic studies. The body temperature is usually normal, sometimes it rises to sub-febrile 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-colored sputum.

On physical examination, a small shortening of the percussion tone and moist rales over the site of infiltration in the lungs can be detected. All of the above symptoms and physical signs disappear quickly, within 1-2 weeks.

Diagnosis of Pulmonary eosinophilic infiltrate:

At x-ray examination non-intense, homogeneous shading of various parts of the lungs without clear boundaries are determined. Shadings can be localized in both or one of the lungs, they can disappear in one place and appear in others. More often the shadows are small, but sometimes they extend to almost the entire lung. In most cases, shading disappears after 6-12 days. The formation of cavities in the lung parenchyma and pleural changes are non-characteristic.

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

The flow must include a destination special means for deworming. Any treatment directed directly at the pulmonary infiltrate is usually not required, since the infiltrate in most patients disappears after a few days and without special treatment. If the manifestations of the disease are pronounced or persist long time may be treated with corticosteroid hormones.

The clinical picture is characterized by a latent onset with the appearance and constant intensification of a cough - dry or with the appearance of a small amount of sputum of a mucous character. Cough is sometimes paroxysmal in nature and is especially pronounced at night. While coughing, some patients develop wheezing and a feeling of shortness of breath. Some patients develop hemoptysis and undetermined chest pain. Lung auscultation reveals scattered dry rales.

In half of the patients on radiographs, diffuse small focal changes in both lungs. Some patients have localized infiltrates in the lungs.

At functional research lung revealed predominantly obstructive changes.

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

Treatment of Pulmonary eosinophilic infiltrate:

Diegylcarbamazine is the most effective antifilarial drug. In some patients, a 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 may occur from exposure to drugs and chemicals. Pulmonary eosinophilic infiltrates that develop under the influence of furadoin, acetylsalicylic acid, azathioprine, chlorpropamide, chromoglycate, isoniazid, metatrexate, penicillin, streptomycin, sulfonamides, beryllium, salts of gold and nickel, and other compounds are described. In addition, eosinophilic pulmonary infiltrates may appear after pollen inhalation of some plants.

The clinical picture of the pulmonary eosinophilic infiltrate that occurs after the use of furadonin is described in particular detail. Lung reactions to furadonin are acute and chronic. In an acute variant of the reaction, fever, dry cough, runny nose, shortness of breath appeared 2 hours to 10 days after the start of furadonin intake. On radiographs, diffuse changes in the lungs are usually detected, sometimes focal irregularly shaped infiltrates in the lungs, there were no rapid disappearance and migration of infiltrates typical of Loeffler's syndrome, sometimes effusion pleurisy appears, and the pleural fluid contains many eosinophils. An increased content of eosinophils in the blood is characteristic. In the acute course of the disease, soon after discontinuation of the drug, the eosinophilic infiltrate in the lung disappears. In the chronic course of the disease, the resorption of the pulmonary eosinophilic infiltrate is delayed, and in some cases pneumosclerosis develops in its place.

Treatment. Acute reactions to drugs and chemical agents do not require special therapy, and the cessation of the action that caused the pulmonary infiltrate factor leads to the complete disappearance of the signs of the disease. In some cases, with a protracted course of the disease, glucocorticosteroid preparations are required.

Pulmonary eosinophilic infiltrates in patients with bronchial asthma in half of the cases are associated with exposure to the patient Aspergillus fumigatus. In some cases, eosinophilic infiltrates are caused by inhalation of plant pollen, house dust, and animal dander. The dryness of the air contributes to the occurrence of this condition, which causes drying of the mucous membrane of the respiratory organs, the formation of thick mucus in the bronchi and a violation of mucus secretion. Changes often occur in patients with bronchial asthma older than 40 years and predominantly in women.

Morphological examination reveals areas of the lungs filled with exudate containing a large number of eosinophils, which are also present in the lumen of the bronchi and sometimes infiltrate their walls.

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

Pulmonary eosinophilic infiltrates occur with systemic lesions connective tissue: periarterin nodosa (see p. 379), Wegener's granulomatosis (see p. 357), J. Churg and L. Strauss syndrome (see p. 384).

Chronic eosinophilic infiltrate(Eckerstroem - Kartagener) which stays the same for weeks and months; it is still so insufficiently delineated that one must be extremely careful with this diagnosis. With this combination of infiltrate with eosinophilia, we are more often talking about a simple coincidence.

Tropical eosinophilic pulmonary infiltrates(pulmonary eosinophilosis or tropical eosinophilia) are endemic in tropical and subtropical countries, especially in India and Africa. Apparently we are talking about infection (Ball, Crofton). Acute and chronic recurrent forms are described with numerous, scattered, small and palm-sized infiltrates in the lungs.

Infiltrates these disappear not as quickly as in Loeffler's syndrome. There is always leukocytosis, sometimes very high, and more or less significant eosinophilia (up to 80%). The titer of the cold agglutination reaction is often increased, in most cases the Wasserman reaction is positive. In contrast to pseudoluetic pulmonary infiltrate with positive reaction Wasserman cases of spontaneous cure is unknown. The disease, however, is well inferior to salvarsan preparations, such as novarsenol, administered at five-day intervals, which can also be used in differential diagnostic terms.
With bronchial asthma sometimes a pulmonary infiltrate is observed simultaneously.
long eosinophilia with long-term non-absorbable changes in the lungs, it raises suspicion of periarteritis nodosa.

Chronic eosinophilic pulmonary infiltrates pathologically occur simultaneously with eosinophilic bone granuloma. You must always look for it true reason- the underlying disease or any complication of pneumonia. Recently, however, Brunner and Tanner were able to show on resected preparations that with differential diagnosis The possibility of chronic pneumonia must be considered if:

a) the history indicates an acute onset of pneumonia without previous symptoms;
b) there is a very high ESR - 50 mm per hour or more (which is especially true against tuberculosis);
c) bronchopneumonic infiltrates of intense density are determined radiographically;
d) increased regional The lymph nodes. The diagnosis must be supported by permanent exclusion of tuberculosis (finding of tuberculous mycobacteria) and cancer (bronchoscopic and cytological findings).

Secondary pneumonia

Secondary pneumonia do not have the characteristic symptomatology common to all of them.
a) congestive pneumonia and pulmonary infarcts are always easy to distinguish from other infiltrates, given the state of the whole organism. Congestive pneumonia is observed mainly on the right, but can be bilateral. The transition to pulmonary edema is gradual. Left-sided pneumonia is rarely due to only one stagnation. Encapsulated interlobar congestive effusion may simulate round shadows of another origin (tumor). Auscultatory with congestive pneumonia, there are always signs of congestive bronchitis with coarse bubbling moist rales.

AT sputum when stained with Prussian blue, the so-called cells of heart defects containing hemosiderin are found.
From other signs hemodynamic heart failure shortness of breath (left ventricular failure) is especially pronounced, while the symptoms of right ventricular failure (congestive liver, edema, etc.) recede into the background. On the part of the blood circulation itself, there are phenomena that cause an overload of the left ventricle (hypertension, aortic insufficiency etc.), mitral valve disease or signs coronary atherosclerosis. Therefore, the heart is almost always enlarged, its configuration is changed, and signs of myocardial damage are noted on the ECG.

b) At lung infarction in the beginning, there is almost always pleural pain, aggravated by breathing and equally frequent both on the right and on the left. Due to sparing during breathing of the corresponding side chest classic auscultatory signs of infiltration are heard only in more late stages. Pleural pain is usually much more intense than with pneumonia. Light to dark red, pure bloody sputum confirms the diagnosis. Bloody sputum in a heart attack is easy to distinguish from rusty sputum with pneumonia. Often, secondary infection of infarcts causes the symptoms observed in infarcts pathological changes blood.

Radiographically almost there are always no classical wedge-shaped shadows given in textbooks with the top facing the roots of the lungs, and the base facing the periphery. To distinguish this shadow from the usual bronchopneumonia radiographically, as a rule, is hardly possible.

It can be said that pulmonary infarction never a primary disease. If there is no phlebitic process, then a previously healthy person should refrain from this diagnosis. On the contrary, the diagnosis of pulmonary infiltrate is too rarely made in bed patients and especially postoperative patients. Changes in the veins are often invisible at first glance, they must be specifically sought. Pelvic vein thrombosis may generally elude clinical examination.

Deep vein thrombosis tend to cause pain on pressure. They sometimes contribute to a noticeable increase in calf volume. Almost all thrombosis begins with these veins. Since pulmonary infarction is a typical secondary disease, then, once it is installed, it is necessary to look for the underlying disease. The figure shows the frequency of various diseases established during autopsy of those who died from pulmonary embolism(Koegel-Zollinger) for a year at the Pathological Institute of San Gallen. heart failure and then malignant tumors are in first place.

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 a longer time or are pronounced, the use of corticosteroids (prednisolone up to 20-30 mg / day) in the form of a short course is justified.

is an allergic inflammation 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; at acute form- with chest pain, myalgia, development of acute respiratory failure. To establish eosinophilic pneumonia, X-ray data and CT scan of the lungs allow, general analysis blood, bronchoalveolar lavage, allergy tests, serodiagnostics. The basis of treatment is specific hyposensitization and hormone therapy.

ICD-10

J82 Pulmonary eosinophilia, not elsewhere classified

General information

The reasons

Eosinophilic pneumonia may result from allergic reaction for taking medications (penicillin, acetylsalicylic acid, sulfonamides, nitrofurans, isoniazid, hormonal and radiopaque drugs, gold compounds), for contact with chemical agents at work (nickel salts). Atopic sensitization of the respiratory tract to fungal spores (especially Aspergillus), flower 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 hypersensitivity reactions immediate type. In addition to hypereosinophilia in the blood of patients, elevated level IgE (hyperimmunoglobulinemia). 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 inflammation lungs may have an asymptomatic course with no or very poor severity of complaints and be determined only by X-ray and clinical and laboratory methods. Loeffler's pneumonia often 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. At chronic form the prolonged existence of infiltrates and relapses contribute to the gradual progression of the disease, the development 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 (reactions of degranulation of basophils and mast cells). Patients with eosinophilic pneumonia usually have a previous allergic history. Auscultation determines a large number of moist finely 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. AT severe cases mechanical ventilation, long-term hormonal therapy are required. With bronchial obstruction, inhaled GCs, beta-agonists are indicated. Expectorants are used for better sputum discharge, breathing exercises. 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 avoids 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, limit contact with aeroallergens, conduct specific hyposensitization. If necessary, it is recommended to change jobs.