Lung infiltration: what is it, what diseases does it occur in? Types of eosinophilic infiltrates. Chronic pneumonia

Lung infiltration - replacement process lung tissue normal airiness area with increased density and an 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 does it occur in?

Pulmonary tissue infiltration syndrome can be a manifestation of various pathological conditions. Most often, an infiltrate in the lungs is formed in the following diseases:

1. Inflammatory processes in the lungs of various natures:

• viral;
• bacterial;
• fungal;
• congestive pneumonia;
• hypostatic pneumonia, etc.

1. Damage to the respiratory system with.
2. Developmental anomalies:

• (pathological anastomosis 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 branching from the aorta);
• (disembryonic formation consisting of elements of the pulmonary parenchyma and bronchial wall).

1. Allergic infiltrate in the lungs.
2. or benign neoplasms.
3. Focal pneumosclerosis.

How it manifests itself

The clinical picture of pulmonary infiltration is determined by the disease that caused pathological process. The severity of symptoms depends on the area of ​​the lesion and the general reactivity of the body. But there are general manifestations of this syndrome, characteristic of any disease that occurs with the formation of infiltrate in the lungs. These include:

• complaints of cough, hemoptysis, painful sensations V chest(with damage to the pleural layers);
• change in general condition (fever, intoxication);
• objective data: lag of half of the chest in the act of breathing (on the “sick” side), increased vocal tremors and dullness of percussion sound over the pathological focus, weakening of respiratory sounds in this area, less often dry and moist rales during auscultation;
• X-ray data: limited or diffuse darkening of the pulmonary field.

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

Infiltration with pneumonia

The inflammatory process in the lungs can be caused big amount various pathogens, and therefore its course has certain differences.

• Staphylococcal differs from other inflammatory processes in the lungs by its tendency to destructive changes with the formation of cavities.
• Pneumonia caused by Klebsiella occurs in weakened 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 lung tissue in the affected area is possible with the formation of thin-walled cyst-like cavities.
• With anaerobic pneumonia, microabscesses form at the site of infiltration, which, merging with each other, break into the bronchus, which leads to the release of foul-smelling sputum with coughing. Often their breakthrough occurs towards the pleura and patients develop empyema.
• Candida 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 sharply during an epidemic. Clinical course it varies from mild forms to fatal outcome. The disease occurs with characteristic symptoms (fever, pain in eyeballs, muscles, adynamia, runny nose). Then comes a paroxysmal cough with sputum mixed with blood and shortness of breath. In the lungs, uneven darkening is detected in the form of foci or affecting the entire lobe of the lungs. Later, nausea, vomiting, and disturbances of consciousness may appear.

The classic course of inflammatory infiltration syndrome can be traced using the example of lobar (lobar) pneumonia.

This pathology is usually caused by pneumococci and has an acute onset. The patient suddenly experiences the following complaints:

• heat body (up to 39-40 degrees);
• chills;
• severe general weakness;
• labored breathing;
• Not productive cough;
• chest pain when coughing and deep breathing.

During this period, swelling of the walls of the alveoli and accumulation of inflammatory exudate in their lumens is observed in the lungs, and the elasticity of the lung tissue decreases. Objective examination reveals typical signs infiltration of lung tissue and additional crepitation of “hot flashes” upon auscultation.

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

Timely treatment in most patients quickly leads to a decrease in intoxication and a decrease in body temperature. During the resolution phase of the process, inflammation in the lesion decreases and exudate gradually resolves. In this case, patients are bothered by a cough with mucus-purulent sputum; on auscultation above the surface of the lungs, moist rales (mostly fine bubbles) and crepitus “low tide” are heard.

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

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

Subsequently, inflammatory infiltrates form in the lungs, which can fester.

Clinically this pathology manifests itself with vague symptoms:

• malaise;
• slight cough;
• chest discomfort.

In some cases it is asymptomatic. The x-ray reveals homogeneous darkening without clear contours, in the blood - high level eosinophils. Such infiltrates can be located in any part of the lungs, either disappearing or appearing again.

Usually the formation of infiltrate in the lungs is preceded by characteristic symptoms(suffocation, cyanosis, chest pain). In this case, the infiltrate has a wedge-shaped shape and its apex is directed towards the root.

Developmental anomalies

Pulmonary tissue infiltration syndrome can be a sign of various developmental anomalies. The latter are most often asymptomatic, so the infiltrate is an incidental finding on an x-ray.

• With sequestration of the lungs, darkening is revealed irregular shape or a group of cysts with a perifocal inflammatory reaction. This pathology can manifest itself during suppuration.
• If there is a hamartoma in the lungs, an infiltrate with clear contours is detected, sometimes with focal calcifications. It is usually located deep in the lung tissue and does not affect the function of the lung tissue. But sometimes a hamartoma is located on the inner surface of the bronchi and can lead to atelectasis and obstructive pneumonia.
• Arteriovenous aneurysms on a radiograph have the appearance of round, clearly contoured shadows, to which lung root dilated vessels are suitable. If the discharge of blood exceeds a third of the total volume of blood flowing through the pulmonary circulation, then the person develops signs of hypoxemia (weakness, decreased ability to work, shortness of breath, etc.).

Lung infiltration in cancer patients

Infiltration in the lungs may be associated with malignant or benign tumor processes. They can long time proceed hidden, revealing itself only when x-ray examination.

Malignant processes should be suspected if an intensively growing formation is detected on the radiograph, having the appearance of a darkening with pitted or blurred edges. Especially high risk The development of this pathology is observed in individuals with a long history of smoking. The first sign of the disease may be intoxication syndrome, as the tumor grows, characteristic pulmonary symptoms (painful cough, shortness of breath, hemoptysis). When a bronchial tube is blocked by a growing tumor, a

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

Causes

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. Pulmonary infarction.
7. Systemic connective tissue diseases.

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

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

Clinical signs

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

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

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

Differential diagnosis of pulmonary infiltrates

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

The first thing you should pay attention to is fever:

• If this is absent, then a nonspecific inflammatory process in the lungs is unlikely. This course is typical for pneumosclerosis or a tumor process.
• If there is fever, it may be pneumonia, lung abscess in the infiltration stage, 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 an area of ​​“darkening” on an x-ray, but also to evaluate its size, shape and intensity.

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

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

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

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

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

Lung infiltration syndrome in lobar pneumonia

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

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

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

Infiltrative form of tuberculosis

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

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

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

Eosinophilic pulmonary infiltrate

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

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

The reasons for this condition may be:

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

Pneumonia due to pulmonary infarction

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

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

They usually have venous thrombophlebitis lower limbs.

Pneumonia due to obstruction of the bronchus by a tumor

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

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

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

Infiltration in pneumosclerosis

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

LESSON No. 5

DIFFERENTIAL DIAGNOSIS OF NON-INFLAMMATORY INFILTRATES IN THE LUNG

Tuberculosis infiltrate is a bronchopneumonic inflammatory focus in the lung. In its center, caseosis, characteristic of tuberculous inflammation, is determined. Caseous necrosis can be mild and sometimes leads 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 infiltration is preceded by fresh focal tuberculosis. Infiltrative pulmonary tuberculosis can occur as a result of lymphobronchogenic spread of mycobacteria from caseous lymph nodes of the mediastinum. Often such patients also have endobronchitis. The infiltrative process is often localized in the middle and lower parts of the lungs.

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

Cloud-shaped, characterized by the presence of a gentle, low-intensity homogeneous shadow with indistinct, blurry contours;

Round (Assmann type) - a round-shaped homogeneous shadow of low intensity with clear contours;

Lobitis is an extensive infiltrative process that involves an entire lobe of the lung, a shadow most often of an inhomogeneous nature, often with the presence of single or multiple decay cavities;

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

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

All clinical and radiological variants are not only characterized by the presence of an infiltrative shadow, often with decay, but also bronchogenic contamination is possible. Often, patients with infiltrative tuberculosis have various types of endobronchitis. If the patient has extreme severe course infiltrative tuberculosis, characteristic of infiltrative-caseous and caseous pneumonia, this should be reflected in the diagnosis. In the first days, with the rapid liquefaction of the resulting caseous masses, a giant cavity or multiple small cavities are formed, in this case the diagnosis is confirmed both by the dynamics of the process and by the abundant bacterial discharge that appears.

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 experience sweating, decreased performance, and a cough that is not painful and does not always attract the patient’s attention, as with focal tuberculosis lungs, but is mostly accompanied by sputum production.

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 detected. After starting treatment, wheezing quickly disappears. With extensive infiltrates, there may be dullness in the corresponding areas of the lungs and 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. Patients with infiltrative pulmonary tuberculosis, as a rule, do not have high leukocytosis with increase in ESR, while in patients with pneumonia, leukocytosis and a shift to the left are typical signs.

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

There are two main variants of the course of infiltrative pulmonary tuberculosis:

A 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 detected wheezing). In the absence of treatment, after some time, patients resume “chest” symptoms and intoxication, i.e., an exacerbation develops. This entire wave-like process is accompanied by the formation of a cavity and continued bacterial excretion;

Involutive course that occurs under conditions of rational treatment. It is characterized by the gradual disappearance of the clinical manifestations of the disease and the earlier disappearance of “chest” symptoms, and then symptoms of intoxication, a subjective feeling of restoration of health, usually within the first 3 months - the cessation of excretion of Mycobacterium tuberculosis in the 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 already formed.

Eosinophilic pulmonary infiltrate

(synonymous with eosinophilic pneumonia) is one of the forms of Loeffler's syndrome. It is characterized by the detection of an infiltrative shadow on an x-ray of the lung, eosinophilia of the blood, 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 incidence of the disease; apparently it occurs quite often. Eosinophilic infiltrate is an allergic disease. Among the agents that cause it are various medications, vaccines, helminthic, microbial and plant allergens. The infiltration is usually discovered incidentally. Some patients complain of feeling unwell, low-grade fever, cough, discharge of mucous or mucopurulent sputum, which may have a canary color, metallic taste and contain blood. Occasionally, a 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 Article 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-Leyden crystals are sometimes found in sputum. The thought of an eosinophilic infiltrate should arise if pronounced and apparently fresh radiological changes in the lungs are accompanied by eosinophilia. The diagnosis is confirmed if after a few days the shadows found disappear. It is supported by the presence of other allergic diseases in the patient in the past or present, the absence of tuberculosis pathogens in the sputum and sometimes negative results of tuberculin tests. Diagnosis is more difficult in severe or prolonged course of eosinophilic infiltrate and in its combination with other lung diseases. The prognosis is favorable, although relapses are possible. Treatment consists of a gentle regimen and, if possible, elimination of the active allergen.

Pulmonary embolism(PE) - blockage of the pulmonary artery or its branches by blood clots, which often form in the large veins of the lower extremities or pelvis (embolism). A broader concept is widespread in foreign literature pulmonary embolism, which also includes rare air emboli, fat emboli, amniotic fluid embolism, foreign bodies, and tumor cells.

Causes and risk factors

The disease is based on thrombus formation, 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.

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

When the endothelium is damaged, the subendothelial zone is exposed, which triggers a cascade of blood clotting reactions. The reasons for this are direct damage to the vessel wall during the installation of intravascular catheters, filters, stents, vein replacement, trauma, and surgery. Hypoxia, viruses, and endotoxins also cause damage to the endothelium. During a systemic inflammatory reaction, leukocytes are activated, which, by attaching to the endothelium, damage it.

The source of blood clots in PE most often are the veins of the lower extremities (lower extremity venous thrombosis), much less often - the veins of the upper extremities and the right side of the heart. In pregnant women, as well as in women who have been taking oral contraceptives for a long time.

Pathogenesis

Embolization is caused by blood clots freely located in the lumen of the vein, attached to its wall only in the area of ​​its base (floating blood clots). The detached thrombus flows through the right side of the heart into 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 body's thrombolytic system.

Thromboembolus

For emboli small sizes no symptoms. Large emboli impair the perfusion of segments or even entire lobes of the lung, which leads to impaired gas exchange and the development of hypoxia. In response to this, the lumen of the vessels of the pulmonary circulation reflexively narrows, and the pressure in the pulmonary arteries increases. The load on the right ventricle 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 infarction 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 manifests itself as 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

PE is often asymptomatic. But the clinical manifestations that arise are nonspecific, which makes diagnosis difficult.

Massive pulmonary embolism is manifested by acute right ventricular failure with the development of shock and systemic hypotension (low 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).

During auscultation of the heart, an increase and accentuation of the second tone over the tricuspid valve and pulmonary artery is detected, as well as a systolic murmur at these points. Splitting of the second tone and gallop rhythm are possible, which is considered a bad prognostic sign. In the area of ​​pulmonary infarction, weakened breathing, moist rales and pleural friction noise are heard.

Diagnostics

Diagnosis is difficult because the symptoms of PE are not specific and diagnostic tests are imperfect. Standard testing (routine laboratory tests, electrocardiography (ECG), chest x-ray) is useful only to exclude other pathologies (eg, pneumonia, pneumothorax, rib fractures, myocardial infarction, pulmonary edema). Sensitive and specific methods for diagnosing PE include determination of d-dimer, echocardiography, computed tomography (CT), ventilation-perfusion scintigraphy, angiography of pulmonary vessels, as well as methods for diagnosing deep vein thrombosis of the lower extremities (ultrasonography, CT venography).

Determination of d-dimer levels

D-dimer is a 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 pulmonary embolism. This means that increased levels of d-dimers occur in a wide variety of other pathological conditions (eg, infection, inflammation, necrosis, aortic dissection). However, normal levels of d-dimers (<500 мкг/л) позволяет исключить ТЭЛА у пациентов с низкой и средней вероятностью.

Electrocardiography

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

Signs of pulmonary embolism on the electrocardiogram are not specific and are absent in most patients. Sinus tachycardia and a tall and pointed P wave (P-pulmonale, a sign of right atrium overload) are often detected. Approximately 20% of patients may exhibit signs of acute cor pulmonale (right ventricular overload): deviation of the electrical axis of the heart to the right; S I Q III T III syndrome (McGinn-White syndrome) - deep S wave in lead I, pronounced Q wave and negative T wave in lead III; new right bundle branch block; 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, severe attack of bronchial asthma).

X-ray of the chest organs

An X-ray of the chest organs reveals signs of pulmonary hypertension of thromboembolic origin: high standing of the dome of the diaphragm on the affected side, dilation of the right heart and roots of the lung, Pall's sign (dilation of the right descending pulmonary artery), Westermarck's sign (English) Russian. (local depletion of the vascular pattern of the lung), discoid atelectasis. For pulmonary infarction - Hampton's triangle (English)Russian. (a cone-shaped compaction with the apex facing the hilum of the lungs), pleural effusion on the affected side.

Ultrasound examination of the 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 are the source of thromboembolism. For this, two methods are used. The first is compression ultrasound; in this case, in B-mode, a cross-section of the lumen of arteries and veins is obtained. Then the ultrasound sensor is pressed on the skin in the projection of the blood vessels. If there is a blood clot 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 speed of blood flow in the vessels is determined. A decrease in the speed of 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.

Pulmonary candidiasis

Pathogen: yeast-like fungus of the genus Candida. The most important are Candida albicans and Candida tropicans. Candidiasis is widespread, but is more common in tropical areas. 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 through the use of common household items (bath, linen, etc.).

Pathogenesis

Candida fungi are commonly found in the mouth, stool, and vagina. Local factors, as well as factors depending 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 injury or surgery, with prolonged use of catheters and burns. Patients with diabetes, HIV infection, oncohematological diseases, pregnant women, and those undergoing antibiotic or glucocorticoid therapy are in a potentially endangered situation. Candidiasis is a common complication of neutropenia, thereby 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. Primary usually occurs in acute form, secondary - in chronic form. 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, and headache. Body temperature usually remains normal. In some patients, the disease begins acutely with a rise in temperature to high numbers. A “scratching” dry cough and chest pain associated with breathing appear. With a mild course in the initial stage, the disease resembles bronchitis with a strong cough without sputum or with scanty, grayish-colored, sometimes yeast-smelling sputum, with dry and moist large- and medium-bubble rales. In more severe cases and at a later date, it may manifest itself as focal or lobar pneumonia, characterized by unstable volatile infiltrates. 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, and often dull chest pain.

Diagnostics

Changes in the hemogram are uncharacteristic. Possible leukopenia, basophilia, eosinophilia, neutrophilia, monocytosis and lymphopenia. X-ray picture. The radiograph reveals multiple spotty shadows caused by small pneumonic foci and atelectasis. Larger lesions are usually located in the lower parts of the lungs. Sometimes miliary shadows (“snow flakes”) appear. The roots of the lung are expanded. Sometimes heavy shadows from foci of shading are found, going to the hilar lymph nodes. The cavernous form is characterized by the appearance of thin-walled cavities and their relatively rapid regression until complete disappearance under the influence of antifungal treatment. Specific diagnostics is based on the isolation of the pathogen from sputum, bronchial secretions and respiratory tract lavages. The complement fixation reaction, the agglutination reaction, is used. The fluorescent antibody method is highly sensitive. An intradermal test with a candida allergen is used.

Treatment

For cutaneous candidiasis, local treatment is carried out with nystatin powder or cream containing ciclopirox. Candidiasis of the oral mucosa responds to tablets with clotrimazole (5 times a day) better than to a suspension with nystatin. Ketoconazole 200-400 mg/day or fluconazole 100-200 mg/day are effective for esophageal candidiasis. In severe cases, amphotericin B 0.3 mg/kg per day is used intravenously for 5-10 days. For HIV infection, fluconazole is considered the most effective drug in the treatment of candidiasis of the oral cavity and esophagus. For candidiasis of the bladder 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 prescribed oral fluconazole. For the disseminated form, amphotericin B at a dose of 0.4-0.5 mg/kg per day or a double dose every other day is the drug of choice. Flucytosine 100-150 mg/kg per day is added to 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 hepatic candidiasis if they do not have neutropenia. Candida krusei is resistant to fluconazole.

Pulmonary aspergillosis

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

Pathogenesis

The disease is caused by inhalation of fungal spores, followed by penetration into the lungs of patients with immunodeficiency. In 90% of patients at risk of developing infection, there are 2 or 3 factors: less than 500 granulocytes, taking high doses of glucocorticoids, or treatment with cytostatics (azathioprine). Invasive aspergillosis can occur during HIV infection, usually with T-helper cell depletion and neutropenia. Characterized by spread through blood vessels, the occurrence of tissue necrosis and hemorrhagic infiltrates. Aspergillus can also spread along damaged bronchial trees and colonize uninfected cysts in the lungs or cavities. It often occurs as a secondary disease in weakened, exhausted patients, especially against the background of diabetes, tuberculosis, blood diseases, and immunodeficiency states. The occurrence is also facilitated by long-term therapy with antibiotics, corticosteroids, and immunosuppressants. In most cases, aspergillomas arise in sanitized tuberculous cavities, cavities after abscesses, bronchiectasis and are a tangle of fungal threads. Localized in the upper parts of the lungs, most often on the right.

Clinic

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

Diagnostics

Drusen and Aspergillus mycelium are isolated in sputum. Repeated isolation of Aspergillus from sputum indicates colonization or infection. In the blood - leukocytosis, eosinophilia, increased ESR. A chest x-ray reveals small foci, partially compacted, sometimes calcified, against the background of pneumosclerosis and compaction of the roots of the lungs. In some cases, the lesions have the character of spherical formations, reminiscent of tuberculoma. Diagnosis requires a biopsy to prove tissue damage and a positive culture result. Blood cultures are rarely positive. Serum IgG antibodies to Aspergillus can be detected in patients with colonization and in almost all patients with balls of fungal filaments.

Complications

Lung abscess. The course of the disease is severe, high fever, shortness of breath, chest pain, hemoptysis. Characterized by increasing weakness, anorexia, increased body temperature, chills and significant sweating often occur. The main symptom is a severe paroxysmal cough with the release of copious bloody sputum containing greenish flakes (clusters of fungal mycelium) 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 fungi are found. Pleural fluid culture is positive for fungal infection. Positive precipitation reaction when examining exudate with a specific antiserum. Calcium oxalate crystals are found in the pleural fluid.

Eosinophilic pulmonary infiltrate is an inflammatory reaction of the lung tissue of an allergic nature to various irritants and antigens.
In this case, transient infiltrates are formed in the lungs, which contain a large number of eosinophils, and the number of these cells is also characteristically increased in the blood.

Etiology. Helminth larvae migrate through the lungs: intestinal eels, roundworms, hookworms. Allergens also influence the occurrence of the disease - pollen of certain plants, occupational allergens in various hazardous industries, fungal spores. Some cases of the disease are diagnosed in connection with the intake of medications (sulfonamides, nitrofurans, penicillin, b-blockers, intal), in connection with the intake of foods - crayfish, eggs, meat, fish. The disease can also be caused by bacteria - streptococcus, brucella, staphylococcus.

Pathogenesis . Infiltrates in the lungs are formed as a result of their attraction from the bloodstream by factors: histamine; eosinophilic chemotactic factor of anaphylaxis; some lymphokines. Allergic reactions of types I, III and IV take part in the formation of eosinophilic infiltrates.

Symptoms Most often, patients do not complain of anything, and infiltrates in the tissues of the patients’ lungs are detected during an X-ray examination, by chance. Sometimes patients complain of coughing, slight weakness, increased body temperature, there may be slight manifestations of asthma, and a small amount of sputum is released when coughing. When listening to the lungs, you can sometimes hear moist fine rales. A blood test reveals moderate leukocytosis with high eosinophilia (up to 70%). Eosinophilia reaches its maximum when infiltrates appear in the lungs.
X-rays show single or multiple infiltrates of unclear contours. Infiltrates are most often found subpleurally in the upper sections. A characteristic symptom of the disease is that infiltrates may disappear a few days after their appearance. If the infiltrate persists for more than four weeks and does not gradually begin to disappear, then this diagnosis is not correct and it is necessary to examine the patient further until the correct diagnosis is made.

TREATMENT

Assign antiallergic, desensitizing treatment. Prednisolone 20-25 mg per day, then gradually reduce the dose. Other corticosteroids (dexamethasone, triamcinolone), pipolfep, suprastin, diphenhydramine, and large doses of calcium may also be prescribed.
Glucocorticoids are not prescribed early, as they interfere with making a correct diagnosis.
In case of helminthiasis, deworming of the patient's body is carried out. If there are manifestations of asthma, then take aminophylline orally and b-adrenergic stimulants by inhalation.