Residual changes after tuberculosis. Residual changes in the lungs after recovery from tuberculosis

3.1. CLINICAL CLASSIFICATION OF TUBERCULOSIS

The basis clinical classification tuberculosis used in Russian Federation, the following principles are laid down:

1. Clinical and radiological features of the tuberculosis process (including localization and prevalence).

2. Phases of its course.

3. Presence of bacterial excretion.

The classification consists of four main sections:

1. Clinical forms of tuberculosis.

2. Characteristics of the tuberculosis process.

3. Complications of tuberculosis.

4. Residual changes after cured tuberculosis. Clinical forms of tuberculosis vary in location and

clinical and radiological signs, taking into account the pathogenetic and pathomorphological characteristics of the tuberculosis process.

Tuberculosis intoxication in children and adolescents.

Respiratory tuberculosis:

Primary tuberculosis complex.

Tuberculosis of the intrathoracic lymph nodes.

Disseminated pulmonary tuberculosis.

Miliary pulmonary tuberculosis.

Focal pulmonary tuberculosis.

Infiltrative pulmonary tuberculosis.

Caseous pneumonia.

Pulmonary tuberculoma.

Cavernous pulmonary tuberculosis.

Fibrous-cavernous pulmonary tuberculosis.

Cirrhotic pulmonary tuberculosis.

Tuberculous pleurisy (including empyema).

Tuberculosis of the bronchi, trachea, upper respiratory tract.

Respiratory tuberculosis combined with occupational lung diseases (coniotuberculosis). Tuberculosis of other organs and systems:

Tuberculosis meninges, central nervous system. Tuberculosis of the intestines, peritoneum and mesenteric lymph nodes.

Tuberculosis of bones and joints. Tuberculosis of the urinary and genital organs. Skin tuberculosis and subcutaneous tissue. Tuberculosis of peripheral lymph nodes. Tuberculosis of the eye. Tuberculosis of other organs.

Characteristics of the tuberculosis process is given according to the localization of the process, clinical and radiological signs and the presence or absence of Mycobacterium tuberculosis (MBT) in the diagnostic material obtained from the patient.

Localization and prevalence are indicated:

In the lungs by lobes and segments;

According to the location of the lesion in other organs. Phase:

a) infiltration, decay, contamination;

b) resorption, compaction, scarring, calcification. Bacterial excretion:

a) with the isolation of Mycobacterium tuberculosis (MBT+);

b) without isolating Mycobacterium tuberculosis (MBT-). Complications of tuberculosis:

Hemoptysis and pulmonary hemorrhage, spontaneous pneumothorax, pulmonary heart failure, atelectasis, amyloidosis, fistulas, etc.

Residual changes after cured tuberculosis:

A) respiratory organs:

Fibrous, fibrous-focal, bullous-dystrophic, calcifications in the lungs and lymph nodes, pleuropneumosclerosis, cirrhosis, condition after surgical intervention and etc.;

b) other organs:

Scar changes in various organs and their consequences, calcification, condition after surgical interventions.

3.2. CLINICAL CLASSIFICATION OF RESPIRATORY ORGAN TUBERCULOSIS

3.2.1. TUBERCULOSIS INTOXICATION IN CHILDREN AND ADOLESCENTS

Primary forms of tuberculosis develop following first infection of the body with MBT.

Primary tuberculosis affects mainly children and adolescents and much less often adults.

From the moment of introduction of tuberculosis infection to the manifestation of tuberculosis as a disease, a period of so-called latent infection passes.

The period of primary infection has characteristic features:

1) high sensitization of the body;

2) a tendency to generalize the process through the lymphohematogenous route;

3) involvement in the process lymphatic system;

4) a tendency to caseous degeneration of the lymph nodes;

5) ability for spontaneous healing.

Tuberculosis intoxication as an independent disease characterizes a period of illness without a clear localization of tuberculosis, and its clinical manifestations reflect functional disorders in various body systems.

Identify the localization of tuberculosis lesions due to their small size, available x-ray and other methods impossible. Most often, the source of intoxication is minimal tuberculous foci in the lymph nodes, especially the mediastinum. Less commonly, lesions are located in the liver, bones, tonsils, etc.

The diagnosis of tuberculosis intoxication is established on the basis of tuberculin diagnostic data (positive, increasing during observation and hyperergic reactions to tuberculin), clinical signs diseases in the absence of local manifestations determined by x-ray and other research methods.

The specificity of the described functional disorders must be confirmed by a thorough examination of the child (adolescent) to exclude nonspecific diseases. During the examination

it is necessary to use modern radiation methods diagnostics, including, if possible, computed tomography, bronchoscopy, complex tuberculin diagnostics, as well as bacteriological examination.

The diagnosis of tuberculosis intoxication is established only after examination in a specialized anti-tuberculosis institution.

Diversity clinical manifestations primary tuberculosis expands due to paraspecific changes in the body:

1) keratoconjunctivitis;

2) erythema nodosum (eritema nodosum);

3) rheumatoid Ponce;

4) acute diffuse nephritis.

In the clinic of tuberculosis intoxication, two periods are distinguished - early and chronic.

Early tuberculosis intoxication in children and adolescents

Symptoms of early tuberculosis intoxication manifest themselves primarily in imbalance of the nervous system, expressed in changes in the child’s behavior: irritability, excitability, decreased attention, sleep disturbances and headaches.

Often during this period it is noted poor appetite, pallor skin, intermittent low-grade fever, some swelling of the external lymph nodes. In thin children, it is easy to palpate an enlarged liver and spleen. There may be indigestion: weakening of the intestines or constipation.

4-6 weeks after primary infection, children develop a positive tuberculin test (turn of tuberculin test).

Often found erythema nodosum (erythema nodosum).

(Figure 3-1, see inset). Its appearance is preceded by a high temperature, a few days after which, mainly on the front surfaces of the legs, dense infiltrates appear, hot to the touch, very painful, red, with a cyanotic tint. Most often, erythema occurs in preschool children and junior schoolchildren, being an allergic, paraspecific reaction, and not a tuberculous skin lesion. It accompanies primary tuberculosis or an outbreak and is considered a manifestation

high allergies onset of the primary disease. Most often it is found on the front surfaces of the legs in the form of painful reddish swellings. The boundaries of the erythema are either clearly defined or appear diffuse. Erythema nodosum never ulcerates (unlike erythema induratum). More often, nodes appear on the skin in the area tibia, less often on the forearms and last from 3 to 6 weeks. Erythema nodosum is a reaction to various factors. In first place is tuberculosis, which can be observed with sarcoidosis. Rheumatism may also be accompanied by erythema nodosum. Periarteritis nodosa produces similar nodes.

The most important differential diagnostic sign of early tuberculosis intoxication is the coincidence of these functional disorders and morphological changes with the variation of tuberculin reactions.

If this period is unnoticed by the parents and the doctor, the child may develop a tuberculosis process in the lungs involving regional lymph nodes or damage to other organs. If the patient receives rational anti-tuberculosis therapy in a timely manner, then all phenomena subside quite quickly and then disappear; only a moderate positive tuberculin test remains.

During this period, the child must be provided with a sanatorium-hygienic regime at home or in medical institution- hospital, sanatorium kindergarten, forest school. Against the background of a properly adjusted diet, rich in the entire complex of vitamins, depending on the severity of intoxication, it is necessary to carry out antibacterial therapy. Treatment should be long-term and continue after the symptoms of early intoxication have subsided.

Chronic tuberculosis intoxication in children and adolescents

characteristic signs are the child's developmental delay, pallor, micropolyadenia(6-9 groups of enlarged lymph nodes are palpated - from elastic consistency to pebbles).

In case of chronic tuberculosis intoxication, it is important that 1 year or more has passed after the change in tuberculin tests, and tuberculin tests remain positive or increase.

For chronic tuberculosis intoxication morphological changes of a tuberculous nature are detected in one or

several organs: V bone marrow, lymph nodes and sometimes in parenchymal organs.

Unlike early tuberculosis intoxication, with chronic intoxication all symptoms are more pronounced and more persistent.

Patients have chronic conjunctivitis, conflicts, which appear and disappear.

Appetite is sharply reduced. Sometimes there are dyspeptic symptoms or constipation. Depending on the duration of chronic tuberculosis intoxication, retardation of physical development, growth and especially body weight child.

As a rule, there is a decrease in turgor of all tissues, skin, and subcutaneous tissue.

There is a slight periodic temperature increase with fluctuations from 37 to 37.5 °C.

The reaction of a sick child to noisy games, favorite activities, and communication with children changes dramatically. As a rule, children get tired quickly, seek privacy and, which is not typical children's age, often go to bed early. Schoolchildren become distracted.

Neither clinically nor radiologically it is possible to detect obvious pathological changes in the lungs. In “older” children, who are carriers of long-term chronic tuberculosis intoxication, a healed primary complex can be detected: a Gon lesion and cicatricial changes in the root with petrification in it.

Chronic tuberculosis intoxication can be prevented correct and long-term treatment. Treatment of already developed chronic tuberculosis intoxication is very difficult. Due to the formation of a fibrous capsule and avascular zone around the lesion, anti-tuberculosis drugs do not fully saturate the tuberculosis lesion, and the MBT located in it do not lose viability.

3.2.2. PRIMARY TUBERCULOSIS COMPLEX

The pathological anatomy of the primary tuberculosis complex is presented in Chapter 1. Etiology and pathogenesis of tuberculosis.

Clinic. In children infancy, in conditions of massive tuberculosis infection, the primary tuberculosis complex proceeds

type of pneumonia, with extensive damage to the intrathoracic lymph nodes. The disease develops with high fever and an increase in temperature to 39-40 ° C, complaints of cough, dry or with the release of mucous sputum, chest pain.

Pneumonia (lobar or segmental) takes on a diffuse character, which depends on hyperergic reactions and incomplete differentiation of the lungs in children. In older children, small primary foci form in the lungs, and in some, various complications of the primary tuberculosis complex are detected.

When examining a child, enlarged peripheral lymph nodes (cervical, axillary) of a dense elastic consistency, mobile, without perifocal inflammation in the surrounding tissue are found. With a large pneumonic focus, there is a lag in the act of breathing of one half of the chest; above it there is dullness of percussion tone; Moist fine bubbling rales are heard. With small pulmonary foci, there are no physical changes.

In the lavage waters of the bronchi and stomach Mycobacterium tuberculosis is found, which comes not only from infiltrative-pneumonic foci located in the lungs, but also from specific changes in the bronchi.

Blood test reveals moderate leukocytosis with a shift of the neutrophil formula to the left, eosinopenia, monopenia and accelerated ESR.

Diagnostics. To make a diagnosis of the primary complex, anamnesis is of great importance - an indication of contact with bacilli, positive tuberculin tests. Particularly valuable is the variation of tuberculin tests, which, with a fresh and active primary complex, is manifested by hyperergic skin tuberculin reactions.

Of great importance is the examination of sputum, bronchial and stomach lavage waters for the presence of tuberculous mycobacteria. X-ray examination reveals fresh pulmonary lesions with accompanying adenitis.

X-ray picture of the primary tuberculosis complex

The classic primary complex consists of three main elements: the pulmonary, glandular components and the lymphangitis that connects them. However, before bipolarity becomes clear on a dorsal-ventral chest X-ray, there is an infiltrative phase. The infiltrate is a rather intense darkening associated with the root of the lung, sometimes it overlaps the root. As a rule, the infiltrate is not homogeneous. Its boundaries are somewhat blurred. Vessels and bronchi are illuminated through the infiltrate. The size of the infiltrates varies and depends on the degree of lung damage; they can be lobar, segmental and broncholobular. More often, the primary complex is localized in the upper and middle segments of the lungs. As the infiltrate resolves, its subpleural location is more clearly visible.

The primary complex has four stages of development:

I stage - pneumonic(Fig. 3-2a). The X-ray image shows three components of the complex:

1) a focus in the lung tissue measuring 2-4 cm in diameter or more, oval or irregular in shape, of varying intensity (usually medium and even high), with an indistinct, blurred outline;

2) outflow to the root, lymphangitis, which is determined in the form of linear strands from the focus to the root;

3) at the root - enlarged infiltrated lymph nodes. The root appears expanded, its structure is blurred, and the intensity is increased. The contours outlining the lymph nodes are either blurred or enlarged nodes are more clearly outlined.

II stage - resorption(Fig. 3-2b). The focus in the lung tissue decreases, its intensity increases, and the contours become clear. The outflow to the root and infiltration of the lymph nodes are reduced.

III stage - compaction(Fig. 3-2c). At the focal point, a hearth up to 1 cm in diameter remains; calcareous inclusions appear in it in the form of small dots sharp intensity. The same inclusions of lime are noticeable in the lymph nodes of the root of the lungs. Thin strands of lymphangitis are identified between the lesion and the root.

Rice. 3-2. Primary tuberculosis complex:

Stage I - pneumonic (a); Stage II - resorption (b); Stage III - compaction (c); Stage IV - calcification (d)

Stage IV - calcification(Fig. 3-2d). The lesion in the lung tissue becomes even smaller, denser, its intensity is high, the contour is clear, often jagged, uneven. Calcifications also increase in the lymph nodes of the root. Calcifications in some cases appear as a continuous dense formation, in others they have less intense shadows of inclusions, which indicate incomplete calcification of the focus and the preservation of areas of caseosis in them. With a favorable outcome of the primary tuberculosis complex, over time, calcification increases in the center of the former caseosis, located in the peripheral parts of the lungs - until bone tissue appears in some cases. This is the Gon focus (Fig. 3-3).

Rice. 3-3. Gon's outbreak

Rice. 3-4. CT calcification in the mediastinal lymph node

In cases where the primary complex is detected in a timely manner and the patient receives full treatment, complete resorption of pathological changes in the lung tissue and root often occurs, with complete restoration of their original pattern.

The greatest difficulties arise when diagnosing tuberculosis intoxication and minor forms of tuberculosis of the intrathoracic lymph nodes. In the absence of radiographic signs of obvious lymphadenopathy, great diagnostic value is attached to computed tomography (CT), which allows visualization of slightly enlarged lymph nodes and calcium salt deposits (Fig. 3-4).

In minor forms of tuberculosis of the intrathoracic lymph nodes, radiological diagnosis is based on identifying deformation and enrichment (strengthening, redundancy) of the hilar pulmonary pattern as a reflection of congestive lymphangitis, disruption of the structure of the root and blurring of its contours.

Complications of the primary tuberculosis complex

The observed complications in the primary tuberculosis complex are reduced to the progression of the process: involvement of neighboring organs (bronchi, pleura), the formation of destruction in the lung tissue, and the occurrence of lymphohematogenous disseminations (Fig. 3-5, 3-6).

Rice. 3-5. Pleural effusion (2) resulting from rupture of the pulmonary component (1) of the primary complex

Rice. 3-6. Thin-walled cavity (1), formed as a result of destruction of the bronchial wall by the primary process in the lung. Mycobacteria from this cavity can spread to other parts of the lungs

Differential diagnosis the primary tuberculosis complex with nonspecific pneumonia is not complicated.

The onset of nonspecific pneumonia is acute, violent, accompanied by chills and fever up to 39-40 °C. Herpetic eruptions on the lips. Objectively - rich stetoacoustic data: intense dullness of pulmonary sound, increased vocal tremors, bronchial breathing with an abundance of wheezing. The blood picture is characterized by high leukocytosis (15,000-20,000), neutrophilia. Pneumonia occurs with a violent clinical picture and ends in crisis in a short period.

With the primary tuberculosis complex, the general condition is relatively good, hyperergic tuberculin tests, the presence of MBT in the sputum, the presence of paraspecific reactions of the sclera, skin and joints, and slow reverse dynamics of the process are noted.

3.2.3. TUBERCULOSIS OF INTRATHORACIC LYMPH NODES (BRONCHOADENITIS)

Bronchoadenitis- disease of the lymph nodes of the root of the lungs and mediastinum. In this form of primary tuberculosis, the inflammatory process mainly involves the intrathoracic lymph nodes.

According to its anatomical structure, the lymph glandular system of the lung is regional to the lymphovascular system of the lung, and the lymph nodes of the root of the lung - as if collector, where lymph collects. When tuberculosis develops in the lung, the root lymph nodes react to it with an inflammatory process. However, in the lymph nodes of the mediastinum and the root of the lung, pathological processes can occur regardless of the disease in the lungs.

Clinic of tuberculous bronchoadenitis

Tuberculous bronchoadenitis, as a rule, begins with intoxication, with its inherent clinical symptoms: low-grade fever, deterioration of general condition, loss of appetite, loss of body weight, adynamia or agitation of the nervous system. Sometimes sweating and poor sleep are noted.

As it progresses, especially in young children, appears bitonic cough, those. cough of two tones. It is caused by compression

destruction of the bronchi by enlarged lymph nodes containing caseous masses.

In adults, due to the loss of elasticity of the bronchial wall, compression is observed very rarely and occurs only in patients with a long-term disease, when the lymph nodes are massive, dense, and contain caseous masses with elements of calcification. In adults there is dry, paroxysmal, hacking, tickling cough.

It is caused by irritation of the bronchial mucosa or appears due to the formation of a bronchopulmonary fistula. As a result of damage to the nerve plexuses located in the area of ​​tuberculous changes, bronchial spasm may occur.

In young children, the volume of the bifurcation group of lymph nodes rapidly increases, and as caseosis and extensive perifocal reaction accumulate in them, suffocation phenomena may occur. These terrible symptoms of asphyxia are accompanied by cyanosis, intermittent breathing, flaring of the wings of the nose and retraction of the intercostal spaces. Turning the child into a prone position alleviates the condition due to the forward movement of the affected lymph node. Blood tests

- without features compared to hemograms of a tuberculosis patient with a different localization of the lesion. However, with the disintegration of caseous masses of lymph nodes and their breakthrough into the bronchus, higher ESR numbers are observed, leukocytosis increases to 13,000-15,000. Detection of Mycobacterium tuberculosis.

Tuberculosis bacilli can be found in the gastric lavage waters; they are especially often found in sputum and bronchial lavage waters when caseous masses break into the bronchus.

X-ray picture of bronchoadenitis Clinical and radiological bronchoadenitis has two options: infiltrative And tumorous (tumor-like). The infiltrative form is more common (Fig. 3-7, 3-8). After the infiltration phase, with proper treatment

The tumorous form is observed in young children infected with massive infection (Fig. 3-9). Often in this case tumor-

Rice. 3-7. Infiltrative bronchoadenitis. On a survey radiograph, the shadow of the root is expanded, its outer contour is blurred, the structure is blurred, the intensity is increased

Rice. 3-8. Infiltrative bronchoadenitis of paratracheal lymph nodes. On a survey radiograph, the shadow in the area of ​​the paratracheal lymph nodes on the right is expanded, its outer contour is unclear, the structure is blurred, the intensity is increased

Noxious bronchoadenitis occurs accompanied by tuberculosis of the eyes, bones, and skin. During the period of illness, the affected lymph nodes undergo changes typical for tuberculosis

For tumorous bronchoadenitis reverse development is slower. Resorption occurs inside the capsule, caseous masses become calcified. Calcifications are formed in greater quantities than in the infiltrative form, and on the radiograph they take the form of uneven round or oval shadows.

Rice. 3-9. Left-sided tumorous bronchoadenitis, massive enlargement of bronchopulmonary lymph nodes on the left (a - survey image and b - tomogram)

Rice. 3-10. Stage of petrification (calcification) of lymph nodes

Dense areas alternate with less dense shadows. The lesion resembles a mulberry or raspberry (Fig. 3-10).

Complications of tuberculous bronchoadenitis. In a complicated course, massive hilar fibrosis and extensive unevenly petrified lymph nodes containing remnants of caseosis with the presence of MBT are observed, giving the possibility of exacerbation or relapse of the tuberculous process.

With a smooth course and complete resorption of infiltrative processes bronchoadenitis documented by small calcifications and coarsening of the lung root.

Complications of tuberculosis of the intrathoracic lymph nodes

With bronchoadenitis it is possible tuberculous lesions of the bronchi with the formation of glandular-bronchial fistulas(Figure 3-11). In case of complete disruption of bronchial obstruction due to blockage of the bronchus by caseous masses or compression by massive lymph nodes affected by tuberculosis (tumor-like bronchoadenitis), atelectasis of the lung area, collapse of a lobe or segment of the lung (1) located above the site of bronchial blockage may occur. In case of complete disruption of bronchial obstruction due to blockage of the bronchial tube by caseous masses or compression by massive lymph nodes affected by tuberculosis (tumor-like bronchoadenitis), atelectasis may occur (2).

Rice. 3-11. Collapse of a lobe or segment of the lung (1), atelectasis of the lower parts of the lung (2)

A frequent complication may be pleurisy, in particular interlobar effusion. Even after its resorption, a compacted pleura of both lobes remains - the mooring. Subsequently, the mooring becomes somewhat thinner, but such evidence of pleurisy remains for life.

In rare cases, when there is a connection between the affected lymph node and the draining bronchus, emptying from it may occur

caseous masses with the subsequent formation of a lymphogenous cavity at this site.

With chronically ongoing bronchoadenitis, lymphohematogenous contamination, found in both lungs, mainly in the upper lobes.

Treatment of tuberculous bronchoadenitis must be comprehensive, using antibacterial drugs and vitamins against the background of a sanatorium-hygienic regime. During the period of subsidence, the patient can return to his professional work and continue outpatient treatment. Early initiation of treatment for tuberculous bronchoadenitis in children and adults and its continuous implementation over a long period guarantees the patient’s recovery and prevents a complicated course of the disease. Intensive specific and pathogenetic therapy quickly produces good results.

Differential diagnosis. When making a diagnosis, tuberculous bronchoadenitis must be differentiated from bronchoadenitis of other etiologies. It is necessary to thoroughly study the medical history, the presence of contact with a bacillary patient, the nature of tuberculin tests, past diseases that can be associated with tuberculosis intoxication or with minor manifestations of primary tuberculosis. A number of diseases of the intrathoracic lymph nodes have some similarities with tuberculous bronchoadenitis.

Lymphogranulomatosis- tumor damage to lymph nodes. The nature of the damage to the nodes themselves in lymphogranulomatosis differs sharply from their changes in tuberculosis.

With lymphogranulomatosis, the lymph nodes are affected symmetrically, often involving the entire group of peripheral nodes in the pathological process. Tuberculin tests are negative or weakly positive.

Characterized by a wave-like increase in temperature with gradually increasing rises and falls, pain in the chest, limbs and joints.

Blood changes are not similar to those with tuberculosis. Anemia, leukocytosis, neutrophilia and lymphopenia are most often detected.

When treated with antibiotics, therapy does not produce results.

The diagnosis of lymphogranulomatosis is confirmed cytologically by lymph node biopsy.

Besnier-Beck-Schaumann sarcoidosis- a disease characterized by infiltrative changes in the intrathoracic lymph nodes. It occurs mainly at the age of 20-40 years, more often in women.

Sometimes it is difficult to diagnose, since the general condition, despite the duration of the disease, remains good, tuberculin tests are negative. Antibacterial therapy has no effect.

In adults, tuberculous bronchoadenitis should be differentiated from metastases of central cancer and lymphosarcoma.

When making a differential diagnosis between tuberculous bronchoadenitis and hilar form of central lung cancer The following should be taken into account.

Cancer usually develops in older people, predominantly men.

There is a persistent cough, shortness of breath, chest pain, and signs of compression of large vessels.

When cancer metastasizes, enlargement of the subclavian lymph nodes (Virchow's glands) is detected.

Tuberculin tests may be negative.

The diagnosis is confirmed by bronchological examination: the presence of a tumor in the bronchial lumen, and in the biopsy material of the bronchial mucosa - tumor elements.

On a chest x-ray with peripheral development of central lung cancer, intense, irregularly shaped darkening is detected. Tomography reveals the shadow of a tumor in the lumen of a large bronchus, narrowing of its lumen, and enlargement of the intrathoracic lymph nodes.

With endobronchial growth, the tumor early leads to bronchial obstruction, the development of cancerous pneumonitis and atelectasis.

The hemogram is characterized by anemia, a shift in leukocyte formula to the left, accelerating ESR (40-60 mm/h).

Lymphosarcoma, with which it is necessary to differentiate tuberculous bronchoadenitis, manifests itself in various clinical symptoms.

Patients complain of fever, weakness, sweating, and the body quickly becomes exhausted.

Patients with lymphosarcoma, much more often than with tuberculous bronchoadenitis, suffer from painful cough, shortness of breath, severe chest pain.

The hemogram is characterized by severe lymphopenia, sharply accelerated ESR. Tuberculin tests are negative.

All groups of lymph nodes are quickly involved in the malignant process. The peripheral nodes are enlarged and form large packets, they are dense and painless.

Cytohistological examination of the lymph node reveals a large number of lymphoid elements (90-98%), which contain large nuclei surrounded by a narrow rim of protoplasm.

3.2.4. DISSEMINATED PULMONARY TUBERCULOSIS

Disseminated forms of tuberculosis include all disseminated processes in the lungs of hematogenous, lymphogenous and bronchogenic origin.

In accordance with the clinical classification of tuberculosis, hematogenously disseminated forms are divided into three main groups:

1) acute disseminated (miliary) pulmonary tuberculosis;

2) subacute disseminated pulmonary tuberculosis;

3) chronic disseminated pulmonary tuberculosis.

1. Acute miliary pulmonary tuberculosis was known to clinicians earlier than all other forms of hematogenous origin.

In hematogenously disseminated pulmonary tuberculosis, pathophysiological disorders and clinical symptoms are diverse. The clinical picture of miliary tuberculosis is characterized by general intoxication and functional disorders. They will manifest themselves in the form of decreased appetite, weakness, and low-grade fever. Patients have a dry cough. The medical history indicates contact with bacillary patients, previous exudative pleurisy, and lymphadenitis.

At the acute onset of the disease There is a rise in temperature to 39-40 ° C, shortness of breath, dry cough, sometimes with the release of a small amount of mucous sputum. During examination, patients have cyanosis (lips, fingertips).

Percussion a pulmonary sound with a tympanic tinge is detected, hard or weakened breathing is heard on auscultation, a small amount of dry or small moist rales, especially in the paravertebral space.

Spleen and liver slightly enlarged.

A pronounced labile pulse and tachycardia are noted.

Tuberculin tests usually false negative (negative anergy).

Changes in blood characterized by leukocytosis, monocytosis, eosinopenia, neutrophilic shift to the left, increased ESR. Protein is detected in the urine.

X-ray picture miliary tuberculosis in the first days of the disease is expressed by a diffuse decrease in the transparency of the lungs with blurred vascular patterns, the appearance of a finely looped mesh due to inflammatory compaction of the interstitial tissue. Only on the 7-10th day of illness, on a plain radiograph, one can see multiple, round-shaped, well-demarcated and located in a chain foci the size of a millet grain, followed by a total symmetrical seeding of the pulmonary fields in both lungs with small foci of the same type (Fig. 3-12) . All important signs of miliary lung disease can be detected using CT (Fig. 3-13). If the process progresses, the pleura and meningeal membranes are affected.

With the reverse development of miliary tuberculosis, the lesions can completely resolve or calcify. The number of calcified lesions is less than during the period of rash, since focal changes partially resolve.

Rice. 3-12. Acute miliary pulmonary tuberculosis

Rice. 3-13.

Patients with generalized and unrecognized tuberculosis die due to symptoms of severe tuberculosis intoxication, hypoxemia and hypoxia.

Miliary pulmonary tuberculosis often has to be differentiated from typhoid fever. With miliary tuberculosis, as with typhus, there are clearly defined symptoms of intoxication, severe headaches, high fever, delirium, and darkened consciousness. However, a careful analysis of symptoms contrary to typhus will help make the correct diagnosis.

Unlike miliary tuberculosis, typhus begins with gradually developing malaise and an increase in temperature. With typhus, bradycardia is observed, with miliary tuberculosis - tachycardia. Symptoms such as shortness of breath, cyanosis, tachycardia, abnormal type of fever, and absence of dyspeptic disorders testify in favor of tuberculosis and against typhus.

The blood picture also differs in diseases: typhus is characterized by leukopenia and lymphocytosis, tuberculosis - leukocytes within normal limits or leukocytosis up to 15,000-18,000.

The Vidal reaction can resolve doubts: it will be positive only for typhoid fever.

An X-ray of the lungs confirms the suspicion of miliary pulmonary tuberculosis.

At early diagnosis miliary tuberculosis, it is important to examine the fundus, where a rash of tuberculous tubercles is detected relatively early.

2. Subacute disseminated pulmonary tuberculosis. The manifestations of this clinical form of tuberculosis are diverse. Functional disorders resemble the picture of an acute infectious disease, for example, typhoid fever. The disease can occur under the guise of influenza or focal pneumonia.

The reason for patients to visit a doctor is often hemoptysis. Patients also consult a doctor in connection with tuberculosis damage to other organs, for example, the larynx, when hoarseness of the voice and pain in the throat appear when swallowing.

With a limited extent of dissemination, the course of a subacute hematogenous process may occur in the absence of symptoms. The above process is detected during preventive fluorographic examinations. Patients complain of a slight cough with sputum production and fever.

Physically, a slight shortening of the percussion sound is detected in the lungs, a small amount of fine bubble moist rales in the interscapular space, and pleural friction noise are heard on auscultation. When a cavity is formed, as a rule, small and medium bubble rales are heard above the cavity.

Mycobacterium tuberculosis is found in sputum.

Changes in blood manifest themselves in the form of leukocytosis (12,000-15,000), an increase in band neutrophils, lymphopenia, increased ESR (20-30 mm/h).

X-ray examination reveals numerous scattered lesions symmetrically on both sides different sizes, they are located mainly in the upper parts of the lungs (Fig. 3-14). The interstitial tissue of the lungs appears in the form of a compacted finely looped mesh.

In case of unfavorable development of the process focuses increase, merge (infiltrate). Cavities form at the site of infiltration. The process extends to the middle and lower parts of the lungs.

Sometimes, with the progression of disseminated tuberculosis, due to trophic changes in the lungs, disintegration of the lung tissue appears in the form of characteristic multiple thin-walled

Rice. 3-14. Tuberculous miliary dissemination in the lungs on the 10th day of illness. CT

Rice. 3-15. Chronic disseminated tuberculosis (survey direct radiographs): a - compaction phase; b - residual changes after chronic disseminated pulmonary tuberculosis

cavern Usually the cavities are round and identical in shape and size. That's why they are named "stamped". They can be located in a chain, often symmetrically in both lungs.

Damage plays a role in the origin of cavities blood vessels, their thrombosis and obliteration. The nutrition of the affected areas of the lungs is disrupted, and destruction occurs in them.

Under the influence of chemotherapy, the temperature normalizes, the cough and the amount of sputum produced decrease. Functional disorders are eliminated; the hemogram is normalized, bacilli excretion stops. Partial resorption of the lesions occurs. Positive results from treatment are achieved within 9-12 months.

3. Chronic hematogenously disseminated pulmonary tuberculosis develops with a long course of the disease and ineffective treatment. Accompanied by complaints of cough with sputum, shortness of breath, worsening with physical exertion, weakness, adynamia, fever (low-grade fever).

A frequent harbinger of exacerbation of chronic hematogenously disseminated pulmonary tuberculosis is exudative pleurisy. Chronic hematogenously disseminated pulmonary tuberculosis is preceded or accompanied by tuberculosis of the kidneys, bones or other organs.

Physically, in the lungs, in the paravertebral space, scattered dry and fine-bubbling, moist rales and pleural friction noise are heard.

Characteristic is a dysfunction of the nervous system and cerebral cortex: mental lability, irritability, decreased ability to work, loss of sleep, neurotic reactions. Endocrine disorders are observed - hyper or hypothyroidism.

Patients experience hemoptysis and pulmonary hemorrhage, symptoms of obstructive bronchitis with symptoms of bronchospasm. Signs of pulmonary heart failure appear: cyanosis, tachycardia, shortness of breath, congestion in the lungs, liver, kidneys, edema of the lower extremities.

The hemogram shows a nuclear shift of neutrophils to the left, lymphopenia, monocytosis, and accelerated ESR.

Patients become bacillary.

The X-ray picture is characterized by compaction of the connective tissue of the lungs, uneven meshwork and rough heaviness of the pulmonary pattern. Against this background, mainly in the upper parts of the lungs, there are scattered foci of varying polymorphism. In the marginal and lower sections there are signs of emphysema

With the progression of chronic hematogenously disseminated tuberculosis, an increase in shortness of breath, an increase in the amount of sputum, and the appearance of hemoptysis are noted. In the lungs, above the caverns, against the background of bronchial breathing, widespread moist, medium-bubbly rales are heard. Specific damage to the upper respiratory tract, intestines, serous membranes and other organs occurs.

Influenced various methods treatment (chemotherapy, pathogenetic treatment), cough decreases, bacilli secretion stops, fresh lesions and dissemination resolve.

The clinical and radiological picture of various forms of disseminated tuberculosis resembles a number of diseases characterized by focal dissemination in the lungs. These are infectious inflammatory diseases, bacterial, viral, fungal lung infections, reticulosis, collagenosis, lung tumors.

Differentiated diagnosis. The largest group of lung diseases with which disseminated forms of tuberculosis should be compared are lobular bronchopneumonia of various etiologies (post-measles, influenza, septic, etc.).

Treatment. Acute miliary tuberculosis is curable even if the meningeal membranes are affected. Treatment should be comprehensive, taking into account all pathophysiological disorders.

For approximate standardized doses of anti-tuberculosis drugs for chemotherapy of primary tuberculosis, see Chapter. 5.

As a result of treatment, complete resorption of the lesions occurs with the restoration of the normal pulmonary pattern and the normalization of all body functions. In some cases, the lesions partially resolve, and the remaining lesions undergo compaction and calcification.

Treatment of patients with disseminated forms of tuberculosis, as already mentioned, should be comprehensive. Chemotherapy is of primary importance; in the acute phase of the process it is necessary intravenous administration antibacterial drugs. Long-term chemotherapy is indicated until fresh lesions in the lungs completely resolve or harden. Among the pathogenetic agents in the acute period, hormonal therapy is carried out with the prescription of corticosteroids (prednisone, prednisolone).

In patients with subacute and chronic hematogenously disseminated tuberculosis, in the presence of decay, collapse therapy is indicated - the imposition of pneumoperitoneum. If cavities in the lungs persist during treatment, surgical treatment methods are used.

3.2.5. FOCAL PULMONARY TUBERCULOSIS

Summary pathological anatomy focal tuberculosis is presented in section 1.4.

Focal pulmonary tuberculosis is classified as post-primary (secondary), which arose in the body with primary tuberculosis foci that had previously been cured.

Focal pulmonary tuberculosis accounts for about 50% of all newly diagnosed tuberculosis diseases. It can occur without subjective sensations and is detected only during a mass fluorographic examination. But upon additional examination, it is often established that patients did not attach importance to a number of symptoms of tuberculosis intoxication for a long time.

Clinico-radiologically, two forms of focal tuberculosis are distinguished: fresh soft focal and chronic fibrous-focal. During the healing process of various forms of tuberculosis, focal changes are formed. These lesions are replaced by fibrous tissue, encapsulated, and are considered fibrotic residual lesions.

The pathogenesis of focal tuberculosis is different, diverse and complex. This form may be a manifestation of the primary or, more often, secondary period of tuberculosis.

Secondary focal forms arise in adults under the influence of exogenous superinfection or endogenous spread of MBT from latent, previously formed foci. Such lesions contain caseation and MBT and are located in the lymph nodes or in any organ.

During the period of exacerbation of the process, MBT from the foci spreads along the lymphatic tract and small bronchi. Most often, fresh lesions appear in the apices of the lungs. First, endobronchitis develops, then the lesion covers all the small branches of the bronchi in this zone. A cheesy necrosis of the walls of the altered bronchi occurs, followed by a transition to the lung tissue, mainly in the apical region. A small focus such as caseous, acinous or lobular pneumonia is formed. The lymphatic network is involved in the pathological process only around the lesion. Regional lymph nodes usually do not respond to lesions in the lungs. Exudative phenomena are small and quickly give way to a productive reaction.

Hematogenous spread characterized by a symmetrical arrangement of foci, the remains of which are located in the apical regions of the lungs.

Clinical picture. Some patients identified using fluorography actually have no clinical symptoms. However, most of them react to the occurrence of low-spread focal pulmonary tuberculosis with weakness, sweating, decreased ability to work and decreased appetite. Patients complain of heat in the cheeks and palms, short-term chills and low-grade fever during the day. Sometimes observed intermittent cough dry or with scant amount of sputum, pain in the side.

When examining the patient it is noted slight pain in the shoulder muscles on the losing side. Lymph nodes are not changed. In the lungs, there may be a shortening of the percussion sound only when the lesions merge. In the fresh phases of development of focal tuberculosis in the presence of infiltrative changes, when coughing, hard breathing and small, moist single wheezes are heard.

Tuberculin tests usually expressed moderately.

From the blood side nothing characteristic of this form of the disease is noted, and blood changes depend on the phase of the disease. In mild, fresh forms, blood counts are normal, in the infiltration phase the ESR is slightly accelerated, the left shift of the formula reaches 12-15% of band forms, and there is slight lymphopenia.

In case of chronic course of the process focal tuberculosis there is a so-called productive form. Foci of small and medium size (3-6 mm), round or irregular in shape, clearly defined, of medium and sharp intensity are identified.

On the radiograph lesions up to 1 cm in diameter, round or irregular in shape are identified. Their contours can be clear or blurred, the intensity is weak or medium. The lesions are single and multiple, most often located in one lung, mainly in the upper sections: in segments I, II and VI; often merge with each other. Wide linear interlacing shadows are visible around the lesions - lymphangitis (Fig. 3-16-3-18).

With progression, an increase in the number of fresh lesions, increased lymphangitis, and decay cavities appear.

Rice. 3-16. Soft focal pulmonary tuberculosis (scheme)

Rice. 3-17. Soft focal pulmonary tuberculosis in the left lung (overview image and tomogram)

Treatment. With modern antibacterial treatment, fresh tuberculosis lesions and lymphangitis usually resolve within 12 months. On the x-ray, you can see complete restoration of the pulmonary pattern or residual slight heaviness and small outlined lesions. Less often, after full treatment, fresh lesions do not resolve, but are encapsulated, and gross fibrosis develops at the site of lymphangitis.

Rice. 3-18. Focal tuberculosis in segments 1 and 2 of the right and in S of the left lung in the infiltration phase (overview image and tomogram). In these segments, numerous foci of small and medium size, low and medium intensity are identified

3.2.6. INFILTRATIVE PULMONARY TUBERCULOSIS

Infiltrative tuberculosis is considered as a phase of progression of focal pulmonary tuberculosis, in which infiltration and perifocal inflammation are leading. With this form of tuberculosis it is extremely diverse proliferative, tissue reaction of the lungs.

The mechanism and reasons for the occurrence of infiltrates that vary in their course are complex. As a rule, the infiltrative-pneumonic process develops against the background of a hyperergic reaction of the body, hypersensitization of the lung tissue, and great lability of the neurovegetative and endocrine systems.

The following clinical and radiological types of infiltrates are distinguished (Fig. 3-19):

1) broncholobular infiltrate;

2) rounded infiltrate;

3) cloud-like infiltrate;

4) caseous pneumonia.

6) periscissuritis.

Rice. 3-19. Schematic representation of radiological types of tuberculous infiltrates in the lungs

Broncholobular infiltrate- this is a focus located in the cortical sections of the first or second segments of the upper lobe of the lung, irregularly round in shape, with unclear contours, with a diameter of 1-3 cm. When tomography, it consists of 2-3 or several merged fresh foci. It is asymptomatic, without functional changes and bacilli secretion (Fig. 3-20).

Round infiltrate- these are foci of darkening of a round or oval shape, vaguely contoured, with a diameter of 1.5-2 cm, most often located in the I-II or VI segments of the lungs. From them to the root of the lung there is an inflammatory “path”, against which the projection of the bronchus is determined (Fig. 3-21a, 3-21b).

X-ray tomographic examination can reveal inclusions of denser or calcified foci, the presence small cavities decay, pleural changes, scar formations. With the progression of round infiltrates, the area of ​​perifocal inflammation increases, and signs of disintegration of the caseous center with the formation of a cavity appear. The cavity contains sequesters and a small amount of fluid - a pneumoniogenic cavity.

Rice. 3-20.(a-b).

Broncholobular tuberculous infiltrate [overview image (a) + (b) tomogram]. In the upper lobe of the left lung, an irregularly shaped area of ​​infiltration measuring 6X7 cm is identified. The intensity of the area is average, without clear contours Rice. 3-21.

Infiltrative pulmonary tuberculosis [overview image (a) + tomogram (b)]. In the upper lobe of the right lung there are 2 foci measuring 3X3 cm, with uneven contours and a heterogeneous structure. Numerous small focal shadows of medium intensity are detected around.

As a result of bronchogenic seeding, foci of varying sizes appear in healthy areas of the lungs. Cloud-like infiltrate

radiographically it is an uneven darkening, the contours of the shadow of which are blurred

chats, it extends to one or more segments of the upper lobe of the lung (Fig. 3-22). Tuberculous infiltrate resembles the picture of nonspecific pneumonia, but differs from it in the persistence of radiological changes, the tendency to decay and the formation of cavities. Rice. 3-22.

Cloud-like infiltrate in the upper lobe of the right lung [overview image (a) + tomogram (b)]. In the upper lobe of the right lung there are 2 foci measuring 3x4 and 2.5x3 cm, of medium intensity, with uneven and unclear contours, a heterogeneous structure due to decay cavities. There are multiple lesions around- an inflammatory tuberculous process that spreads to the entire lobe of the lung. Lobitis is distinguished by its structural forms (many caseous lesions) and severe clinical picture. As the process progresses, the entire lobe of the lung is affected, which is delimited by a clear interlobar groove. Observations over time have shown that lobita is often preceded by the development of a small infiltrative focus (Fig. 3-23).

Periscissuritis, or regional infiltrate,- This is a cloud-like infiltrate located at the interlobar groove. The apex of the triangle is facing the root of the lung, the base is outward. The upper borders are vague and pass without sharp outlines into slightly changed lung tissue. The lower border corresponds to the interlobar pleura and is therefore clear (Fig. 3-24).

Rice. 3-23. Tuberculosis infiltrate. Infiltrative shadow occupying the lobe of the right lung (lobitis), with an emphasized lower border. The interlobar fissure is shifted upward

Rice. 3-24. Periscissuritis

Caseous pneumonia. In some patients with insufficient immunobiological resistance, the infiltrate takes on the character of caseous pneumonia. Caseous pneumonia is characterized by the development of an inflammatory reaction in the lung tissue with a predominance of necrosis, and caseous-pneumonic foci occupy a lobe and even the entire lung.

The development of caseous pneumonia is facilitated by a number of unfavorable factors: malnutrition, pregnancy, diabetes, massive infection with highly virulent Mycobacterium tuberculosis.

Caseous pneumonia can develop after pulmonary bleeding as a result of aspiration of blood with tuberculous mycobacteria.

The clinical picture of caseous pneumonia is determined by the prevalence and intensity of morphological changes.

Clinic of infiltrative tuberculosis. The severity of clinical symptoms generally corresponds to the extent of specific lesions in the lungs. In most cases, infiltrative tuberculosis begins acutely with a high temperature and can proceed as follows: lobar pneumonia or flu. The clinic of an acute illness appears against the background of complete health. Only with a thorough interview of patients is it possible to identify symptoms of tuberculosis intoxication that appeared before the onset of the acute disease.

Often the first symptom of infiltrative-pneumonic tuberculosis is hemoptysis or bleeding. The duration of the acute period of the disease varies: from several days to several weeks.

From complaints Most often, chest pain is observed on the affected side (in the side or in the area of ​​the shoulder blades), a cough is dry or with scant sputum production. The symptoms of tuberculosis intoxication are pronounced: poor appetite, sweating, sleep disturbance, increased excitability, tachycardia, general weakness.

For caseous pneumonia onset of the disease is acute: from high temperature up to 40-41°C, hectic type, with large differences between morning and evening temperatures. Symptoms of tuberculosis intoxication quickly increase, severe adynamia, profuse sweats, chest pain, cough with purulent sputum, shortness of breath are observed, and patients quickly lose weight.

On physical examination initial signs Infiltrative tuberculosis are: lag of the chest on the affected side when breathing, tension and soreness of the chest muscles, increased vocal tremors.

Percussion and auscultation data acquire a more pronounced character with massive pneumonia such as lobita and with the beginning of disintegration of the infiltrate with the formation of a cavity. At this time, it is possible to determine dullness of percussion over the affected area.

low sound, bronchophony, bronchial breathing, moist, sonorous persistent wheezing of various calibers.

Differential diagnosis of infiltrates. The acute onset of the disease and the rapid development of the pneumonic process in persons who do not have a history of tuberculosis serve as a reason for making a diagnosis of nonspecific pneumonia.

Diagnosis of infiltrative-pneumonic tuberculosis occurring with influenza syndrome is especially difficult. Its important differential diagnostic differences from pneumonia are:

1) signs of tuberculosis intoxication;

2) gradual onset of the disease;

3) absence of catarrhal inflammation of the upper respiratory tract;

4) the relatively satisfactory condition of the patients, despite the high temperature.

With nonspecific pneumonia with high fever, the condition of the patients is severe, while the specific (tuberculosis) process occurs with the absence of physical data at the onset of the disease and their appearance only as the process progresses. In blood tests of patients with tuberculosis, slight shifts in the leukocyte formula and a slight acceleration of the ESR are observed, in contrast to lobar pneumonia, when high leukocytosis with a shift to the left and a sharply accelerated ESR are observed.

X-ray shows that tuberculous infiltrates are localized mostly in the upper sections (I, II and VI segments), and nonspecific inflammatory processes - in the middle and lower fields.

A “path” extends from the tuberculous infiltrate to the root of the lung; Usually, individual focal shadows are visible along the periphery of the main focus of the lesion; the latter may be in other areas of the same or opposite lung as a result of bronchogenic contamination.

In some cases, only dynamic monitoring of the patient’s condition, the lack of effect from treatment with nonspecific antibacterial agents, and the appearance of Mycobacterium tuberculosis in the sputum allow a diagnosis of tuberculosis to be made.

Long-term reverse development of the process makes it possible to distinguish infiltrative-pneumonic pulmonary tuberculosis from eoseptic

nophilic pneumonia, the main symptom of which is the rapid resorption of the focus within a few days. In addition, with eosinophilic pneumonia, eosinophilia in the blood reaches 30-45%. Eosinophilic pneumonia disappears without a trace: after 7-10 days, complete restoration of the lung tissue occurs.

In addition to malignant neoplasms, tuberculous infiltrate sometimes has to be differentiated from pulmonary echinococcus, actinomycosis, lymphogranulomatosis, dermoid cysts, pulmonary syphilis, etc. Only a comprehensive examination of the patient and a thorough analysis of clinical and x-ray laboratory data can correctly recognize the nature of the process in the lung tissue.

Treatment. When infiltrative tuberculosis is detected, treatment begins in a hospital setting with first-line antibacterial drugs using pathogenetic therapy. Treatment of the patient is carried out until complete resorption of infiltrative changes, on average 9-12 months, followed by anti-relapse courses of chemotherapy under clinical observation.

For approximate standardized doses of anti-tuberculosis drugs for chemotherapy of tuberculosis, see Chapter. 5.

The clinical diversity of forms of infiltrative tuberculosis necessitates the integrated use of various treatment methods. In the absence of a long-term effect and the destruction persists, it is sometimes advisable to add collapse therapy (artificial pneumothorax) or surgical intervention.

3.2.7. PULMONARY TUBERCULOMA

A summary of the pathological anatomy of tuberculosis is presented in section 1.4.

Pulmonary tuberculoma unites encapsulated caseous foci of various genesis, more than 1 cm in diameter. Source of formation of tuberculomas There are mainly two forms of pulmonary tuberculosis: infiltrative-pneumonic and focal. In addition, tuberculomas are formed from cavernous tuberculosis by filling the cavity with caseosis.

Filled cavities relate to tuberculomas only conditionally, since the filling of the cavity occurs mechanically, while tuberculomas are a peculiar phenomenon in the lung tissue.

On the radiograph tuberculomas are revealed as a rounded shadow with clear contours. In focus, a crescent-shaped clearing can be determined due to decay, sometimes perifocal inflammation and a small number of bronchogenic foci, as well as areas of calcification (Fig. 3-25, 3-26).

Rice. 3-25. Tuberculoma in the decay phase. On a plain radiograph (a) in the upper lobe of the left lung, a polygonal shadow with clear contours, measuring 6x9 cm of medium intensity, is determined. The tomogram (b) reveals a crescent-shaped clearing due to the disintegration

Rice. 3-26. Multiple tuberculomas with disintegration [overview image (a) + tomogram (b)]. In the upper lobe of the right lung there are multiple rounded shadows with a diameter of 1.5-2 cm of medium intensity, with clearing in the center and clear contours. The presence of decay in tuberculomas is confirmed by tomographic examination

Three clinical variants of tuberculosis have been identified:

1) progressive, which is characterized by the appearance at some stage of the disease of decay, perifocal inflammation around the tuberculoma, bronchogenic seeding in the surrounding lung tissue;

2) stable, in which there are no radiological changes during observation of the patient or rare exacerbations occur without signs of tuberculoma progression;

3) retrogressive, which is characterized by a slow decrease in tuberculoma, followed by the formation in its place of a focus or group of lesions, an induration field, or a combination of these changes.

In relation to all forms of pulmonary tuberculosis, patients with tuberculomas account for 6-10%. This is explained by the fact that extensive infiltrative-pneumonic processes under the influence of treatment and increasing the body's resistance are limited and compacted. However, the process does not stop completely, remaining a clearly defined dense formation.

Clinical picture. Since tuberculoma itself is an indicator of the body’s high resistance, patients with this form of pulmonary tuberculosis are often identified by chance during fluorographic examinations, preventive examinations, etc. Patients make virtually no complaints.

On physical examination The patient's lung pathology is also not detected. Wheezing is heard only during a massive outbreak with widespread infiltrative changes in the lung tissue around the tuberculoma.

Blood picture also without any features; during exacerbations, a moderate acceleration of ESR and moderate leukocytosis are observed.

In stable tuberculomas, MBT is not found in sputum. In the presence of decay in tuberculomas, bacilli discharge occurs in cases where there is a connection with the drainage bronchus.

Tuberculin tests. Patients with pulmonary tuberculomas in most cases react positively to tuberculin; the Mantoux test often has a hyperergic character.

Treatment. Before the discovery of antibacterial drugs, the prognosis for tuberculomas was poor - tuberculomas gave massive outbreaks with subsequent transition to severe forms of pulmonary tuberculosis. Now, in 80% of patients with tuberculomas, the process of regression

persists or occurs chronically without exacerbations. For approximate standardized doses of anti-tuberculosis drugs for chemotherapy of tuberculosis, see Chapter. 5.

When identifying patients with pulmonary tuberculomas, hospitalization and long-term treatment. If decay persists in the tuberculoma for a long time and the patient continues to secrete MBT, and long-term antibacterial therapy does not lead to the desired results, it is recommended to resort to surgical intervention.

Surgery. Usually the operation is performed with minimal removal of lung tissue - segmental resection. Surgical treatment is also indicated in cases where there is no certainty that the patient has tuberculosis, since it can be difficult to distinguish tuberculoma from other lung diseases, especially tumors.

To diagnose tuberculoma, it is necessary to conduct a bronchological examination with a catheterization biopsy, as well as puncture of the bifurcation lymph nodes. These techniques make it possible to make a correct diagnosis in almost 90% of cases.

3.2.8. CAVERNOUS PULMONARY TUBERCULOSIS

A summary of the pathological anatomy of tuberculosis is presented in section 1.4.

Distinctive features of the cavernous form of pulmonary tuberculosis are the presence of a thin-walled cavity located on the

background of little changed lung tissue in the absence of pronounced infiltrative and fibrous changes (Fig. 3-27, 3-28).

Rice. 3-27. Cavernous pulmonary tuberculosis. Overview shot. In the upper parts of the left lung there is a group of formed decay cavities, without a pronounced perifocal zone of inflammation and limited focal contamination

Rice. 3-28. Elastic cavity in the upper lobe of the right lung. A ring-shaped, thin-walled shadow with clear contours, measuring 6x5 cm, is identified. Dense foci and fibrosis are detected in the adjacent part of the lung. Share in size is not reduced

Cavernous tuberculosis develops in patients with infiltrative, disseminated focal tuberculosis during the disintegration of tuberculomas.

X-ray examination reveals a round-shaped cavity with a thin two-layer wall and usual localization in the subclavian region.

There are usually no physical manifestations. Only when coughing at the height of inhalation are individual fine-bubbly moist rales heard. Catarrhal phenomena occur later, with the appearance of perifocal inflammatory changes around the cavity and thickening of its wall.

Changes in blood in patients with cavernous tuberculosis are also less pronounced: the number of leukocytes is normal, ESR is often accelerated (20-40 mm/h).

Mycobacterium tuberculosis and elastic fibers are detected in sputum or bronchial washings. But to detect MBT, it is necessary to use not only bacterioscopy, but also culture methods.

Treatment Treatment of patients with cavernous pulmonary tuberculosis should be comprehensive, including methods of collapse therapy and surgical intervention.

For approximate standardized doses of anti-tuberculosis drugs for chemotherapy of tuberculosis, see Chapter. 5.

Surgical removal of the cavity- this is an important stage in the treatment of patients with cavernous forms.

Combination of chemotherapy with surgical methods treatment provides clinical cure for patients with cavernous forms.

3.2.9. FIBROUS-CAVERNOUS PULMONARY TUBERCULOSIS

A summary of the pathological anatomy of tuberculosis is presented in section 1.4.

Fibrous-cavernous pulmonary tuberculosis- a chronic disease that occurs over a long period of time and in waves, with intervals of subsidence inflammatory phenomena. It is characterized by the presence of one or several long-standing cavities with pronounced sclerosis of surrounding tissues, fibrous degeneration of the lungs and pleura.

Pathogenesis. Pathogenetically, this form does not arise independently, but is a consequence of infiltrative tuberculosis. The hematogenously disseminated form also serves as a source of fibro-cavernous processes in the lungs.

Of course, with an advanced fibrocavernous form, it is not always easy to determine what caused its development.

The extent of changes in the lungs may vary. The process can be one-sided or two-sided, with the presence of one or many cavities.

Fibrous-cavernous tuberculosis is characterized by foci of bronchogenic dropout of varying duration. As a rule, the bronchus draining the cavity is affected. Other morphological changes in the lungs also develop: pneumosclerosis, emphysema, bronchiectasis.

History of patients with fibrous-cavernous lung disease is characterized by complaints about the duration of the tuberculosis disease and its wave-like course. The intervals between the outbreak and clinical relief may be very long, or, conversely, there may be frequent recurrence of outbreaks. In some cases, patients do not subjectively feel the severity of the disease.

The clinical manifestations of fibrous-cavernous tuberculosis are diverse; they are caused by the tuberculosis process itself, as well as developed complications.

There are two clinical variants of the course of fibrous-cavernous pulmonary tuberculosis:

1) limited and relatively stable, when, thanks to chemotherapy, a certain stabilization of the process occurs and exacerbation may be absent for several years;

2) progressive, characterized by alternating exacerbations and remissions, with different periods between them.

During periods of exacerbation, a rise in temperature is observed, which is explained by specific outbreaks of the process and the development of infiltration around the cavity. The temperature can be high in cases where a secondary infection is associated with the disease.

Damage to the bronchi is accompanied by a protracted “nasty” cough, during which viscous mucopurulent sputum is difficult to separate.

Frequent complications are:

1) hemoptysis;

2) pulmonary hemorrhages caused by perforation of large vessels due to the caseous-necrotic process.

The appearance of a patient with long-term fibrocavernous tuberculosis is very characteristic and is called habitus phthisicus. The patient is distinguished by sudden weight loss, flabby dry skin that easily forms wrinkles, muscle atrophy, mainly of the upper shoulder girdle, back and intercostal groups.

Patients suffer from constant intoxication. With frequent outbreaks of the tuberculosis process, respiratory failure II and III degree. Congestion and acrocyanosis are noted. Subsequently, the liver enlarges. Swelling may occur. As the process progresses, specific damage to the larynx and intestines is observed, which leads to a sharp decrease in

body resistance. With the development of cachexia, amyloid nephrosis and pulmonary heart failure, the prognosis becomes difficult.

Percussion gives clearly defined symptoms: shortening of sound in areas of pleural thickening and massive fibrosis. During outbreaks with a significant extent and depth of pneumonic and infiltrative processes, a shortening of the percussion sound can also be noted. There is no pattern in the distribution of these processes, so we cannot talk about their predominant topography.

Auscultation in places of fibrosis and thickening of the pleura, weakened breathing is detected. In the presence of infiltrative-pneumonic exacerbations, bronchial breathing and small moist rales can be detected. Over large and gigantic cavities, bronchial and amphoric breathing and large-bubble, sonorous, moist rales are heard. Above small cavities, wheezing is less sonorous, not abundant, and is better heard when coughing. Above the old cavity, a “creaking cart” and “squeaking” can be heard, caused by cirrhosis of the cavity wall and surrounding tissue.

Thus, during the fibrocavernous process, an abundance of stetoacoustic symptoms can be detected. However, there are “silent” and “pseudonymous” cavities that do not give either percussion or auscultation symptoms.

An x-ray usually reveals a picture of fibrosis and shrinkage of the lung, an old fibrous cavity (one or more), and pleural layers.

X-ray picture fibrosis and shrinkage of the lung is most often found in the upper lobes with a predominant lesion of one of them. The mediastinum and trachea are displaced towards the larger lesion. The upper lobes are reduced in volume, their transparency is sharply reduced due to hypoventilation. The pattern of lung tissue is sharply deformed as a result of the development of severe fibrosis. In the lower parts of the lungs, transparency is often increased, which indicates emphysema. The roots are usually shifted upward. Large vessels are defined as straight, even shadows - the so-called “tight string” symptom. Typically, groups of lesions of varying size and intensity are visible in both lungs

Rice. 3-29. A plain radiograph reveals: a picture of fibrosis and shrinkage of the lung, multiple old fibrous cavities, pleural layers in the upper parts of the left lung

Rice. 3-30. Cavity with liquid level (overview image). In the middle sections of the right lung, a cavity with a diameter of 6x7 cm is identified, which is located among gross fibrosis of the lungs, its walls are deformed and dense. A small level of liquid is detected at the bottom of the cavern

In the fibrous-cavernous process, the cavity is located among severe fibrosis of the lungs, its walls are deformed, dense, and most often thickened. Often, a small level of liquid is detected at the bottom of the cavern (Fig. 3-30). With exacerbation and progression of the process, areas of infiltration are visible around the cavity. During treatment, slow resorption of these changes, partial reduction and wrinkling of the cavity are noted.

Sometimes a fibrous cavity is detected only with tomography, since on a regular radiograph the shadow of the cavity can be covered by overlapping shadows of foci, fibrosis and pleural layers. At laboratory research sputum

constant bacilli secretion is detected, sometimes massive, as well as coral-shaped elastic fibers. Blood.

The state of the blood in patients with fibrous-cavernous tuberculosis depends on the phase of the disease. During an outbreak, it is the same as with active tuberculosis, but with a change in the formula towards lymphopenia, left shift and accelerated ESR to 30-40 mm/h. With severe bleeding, anemia is detected, sometimes very pronounced. With secondary infection, a higher leukocytosis is observed - up to 19,000-20,000 and an increase in neutrophils. In urine

Treatment. with renal amyloidosis, which often develops in patients with fibrous-cavernous pulmonary tuberculosis, the protein content is usually high. Before the use of chemotherapy, the average life expectancy of such patients was limited to 2-3 years. Currently, there are all possibilities to prevent the development of the fibrous-cavernous process. To do this, at the very beginning of one or another form of the disease, good contact between the doctor and the patient must be established. It is equally important that the doctor achieve

full implementation

Healing of cavities with a fibrous wall always proceeds very slowly. If necessary, general therapy is supplemented with surgical intervention. With a unilateral process and good functional indicators, lung resection of varying volumes is performed. Currently, operations with a bilateral process also give in most cases quite satisfactory results: the patient remains able to work, his life expectancy is significantly extended, and the release of mycobacteria stops.

3.2.10. CIRRHOTICA PULMONARY TUBERCULOSIS

A summary of the pathological anatomy of tuberculosis is presented in section 1.4.

Clinical manifestations of cirrhotic tuberculosis diverse.

The most characteristic complaints of patients are progressive shortness of breath and cough with sputum. If at the beginning of the disease shortness of breath appears during physical activity, then later it occurs even at rest. Hemoptysis and pulmonary hemorrhages occur when angioectasia ruptures. Temperature increase

associated with exacerbation of chronic pneumonia or bronchiectasis.

Changes in the hemogram are caused by exacerbations of pneumonia: moderate leukocytosis, acceleration of ESR to 20-30 mm/h.

Percussion When examining the patient, a deformation of the chest is noted: it is flattened, the ribs are slanted, and the intercostal spaces are narrowed. Recession of the supraclavicular and subclavian fossae is noted, the lower parts of the chest are emphysematously dilated.

Auscultation In patients with unilateral cirrhosis, a displacement of the trachea towards the affected lung is determined.

Above the area of ​​cirrhosis, the pulmonary sound is shortened. A box-like tone of sound is detected over areas of emphysematously altered lung tissue. weakened hard or bronchial breathing and dry, scattered, wheezing sounds are heard. Above the bronchiectasis cavities, sonorous moist rales with a “creaky” tint characteristic of cirrhosis are heard. With unilateral cirrhosis, the boundaries of relative cardiac dullness are shifted towards the affected lung.

For X-ray picture

new shadows. The pulmonary roots are pulled upward, and the heart suspended on them has a “droplet/hanging” shape.

Rice. 3-31. Cirrhotic pulmonary tuberculosis (plain radiograph). Massive cirrhosis of the entire right lung, mediastinal shift to the right

Rice. 3-32. Cirrhotic pulmonary tuberculosis (plain radiograph). Massive cirrhosis of the upper parts of the left lung, shift of the mediastinum to the left

Purely cirrhotic forms of the tuberculosis process are rarely observed. Most often, there are peculiar forms of cavernous

no-cirrhotic tuberculosis, when, along with massive cirrhosis in the lungs, decay cavities of various sizes and shapes can be detected. These can be cleaned old cavities, cavities that retain specific inflammatory changes in their walls, and bronchiectasis cavities. Processes of this kind lead to the switching off of the lung from the act of breathing and the complete loss of its function; such a lung is called a “destroyed lung.”

Morphological picture of a “destroyed lung” tuberculosis etiology is characterized by a 2-3 times reduction in the size of the lung compared to the norm, compaction of the lung, fusion and thickening of the pleural layers. A “collapsed lung” develops on one side, most often the left.

Alveolar lung tissue almost completely replaced by fibrous. Against the background of fibrotic changes, there are small and medium-sized cavities and multiple bronchiectasis. Sometimes one or two large cavities are observed on a cirrhotic background.

Depending on the sclerotic changes in the pulmonary parenchyma and cavitary formations, three types of “destroyed lung” of tuberculous etiology can be distinguished:

1. Cavernous-cirrhotic type - one large, “leading” cavity is visible against a cirrhotic background.

2. Polycavernous-cirrhotic type - the presence of many small cavities against the background of cirrhosis of the rest of the lung.

3. Pneumatous-cirrhotic type - complete replacement of the pulmonary parenchyma with fibrous tissue with a large number of bronchiectasis and small residual cavities.

Treatment should be carried out in the following directions:

1) treatment of the underlying pulmonary process;

2) improvement of bronchial obstruction (bronchodilators, expectorants);

3) treatment of pulmonary heart failure. The principles of treatment of tuberculosis are presented in Chapter. 5. Prevention tuberculous cirrhosis consists of the correct and

timely treatment of pulmonary tuberculosis.

3.2.11. TUBERCULOUS PLEURITIS (INCLUDING EMPYEMA)

The diagnosis of pleurisy is established by a combination of clinical and radiological signs, and the nature of pleurisy is determined by the results of a study of diagnostic material obtained during puncture pleural cavity or pleural biopsy.

A summary of the pathological anatomy of tuberculosis is presented in section 1.4.

Pleurisy may be the first clinical manifestation of tuberculosis, especially in adolescents and young adults. It often develops with primary tuberculosis. Pleurisy may be the only clinical manifestation of the disease when it occurs in the presence of hidden fresh lesions located subpleurally in the lungs, or lesions in the lymph nodes.

Clinically, pleurisy is divided into dry and exudative.

According to clinical manifestations, pleurisy is divided into acute, subacute and chronic.

According to localization, the following pleurisy is distinguished:

a) bone-diaphragmatic;

b) diaphragmatic;

c) costal;

d) interlobar;

e) paramediastinal;

e) apical.

More often, the effusion is located freely in the pleural cavity, but it can also be encysted.

Dry (fibrinous) pleurisy is an inflammation of limited areas of the pleura with the deposition of fibrin on its surface. The main clinical manifestations are chest pain, dry cough, general condition and low-grade fever. The localization of pain depends on the location of the lesion. The pain intensifies with deep breathing, coughing and pressing on the intercostal spaces.

On physical examination In patients, there is a lag on the affected side of the chest when breathing, and a slight dullness of the percussion tone.

Auscultation: the main diagnostic sign is a pleural friction noise, which intensifies when pressed with a stethoscope and does not disappear after coughing.

Blood analysis in patients with pleurisy, it reveals moderate leukocytosis, a shift of neutrophils to the left and an acceleration of ESR.

During X-ray examination limited mobility of the dome of the diaphragm is revealed, the contours of the diaphragm become uneven, and the transparency of the affected parts of the lungs decreases.

Dry pleurisy proceeds favorably and ends with a cure. Sometimes it becomes recurrent. Antibacterial treatment is carried out according to standard schemes depending on the resistance of the office and the body’s tolerance to anti-tuberculosis drugs.

Exudative (serous) pleurisy is a common form of pleurisy of tuberculous etiology. It begins gradually with general malaise, weakness, periodic chest pain, occasionally with a cough, and low-grade fever. Then the temperature rises, chest pain intensifies, and shortness of breath appears. As exudate accumulates, shortness of breath increases due to lung collapse and pressure on the mediastinal organs.

Relatively rarely, pleurisy begins during a period of complete health with chills, high fever, chest pain, and a dry, painful cough.

The course of acute serous pleurisy of tuberculous etiology can be divided into three periods: exudation; process stabilization; effusion resorption.

On physical examination patients with pleurisy, in the exudation phase there is a limitation of the respiratory excursion of the affected side, smoothness of the intercostal spaces and even their bulging with large amounts of fluid. Characteristic is dullness of percussion sound with an upper border in the form of an oblique Ellis-Damoiso line, which runs up from the spine, reaches the top point along the axillary lines and then descends in front along the anterior wall of the chest. A shift of the mediastinal organs to the healthy side is usually observed when a large amount of fluid accumulates in the pleural cavity.

Phases of stabilization and resorption of exudate are characterized by subsidence of signs of the disease, a decrease in temperature, a decrease in pain and shortness of breath. Objective pathological symptoms gradually disappear, but a pleural friction rub may appear.

Hemogram changes in the acute phase they are characterized by the presence of leukocytosis (up to 12,000-15,000), lympho- and eosinopenia, a neutrophilic shift to the left and an acceleration of ESR to 50-60 mm/h. As the process subsides, blood counts return to normal.

With exudative pleurisy, significant changes in the proteinogram are noted.

In the acute phase, the amount of albumin decreases and globulins increase. With the involution of the process, the normal content of globulins is restored. If fluid accumulates above the diaphragm, then it is often not visible to the patient in an upright position. In such cases, examination in the lateral position is necessary. As the effusion increases, a homogeneous darkening appears in the area of ​​the external sinus. The pulmonary pattern is poorly differentiated. Free fluid can move depending on the patient's body position. Pleural fluid can accumulate in the interlobar fissures, paramediastinal and in the area of ​​the dome of the diaphragm, where darkening is determined during polypositional x-ray examination (Fig. 3-33, 3-34).

Rice. 3-33. Left-sided exudative pleurisy (overview photo)

Rice. 3-34. Pleural layers (overview image). Residual changes after pleurisy, left

To determine the nature of the exudate and etiology pleurisy is extremely important to study pleural effusion. Serous effusion in tuberculosis is usually transparent, yellowish color, with a specific gravity of 1015 to 1025 and a protein content of 3-6%. In the acute phase of exudation, lymphocytes predominate in the effusion (50-60%),

there are small numbers of eosinophils, red blood cells and mesothelial cells.

With tuberculosis, cholesterol pleurisy with yellow-green or yellow effusion may be observed. Brown containing significant amounts of cholesterol. Such effusions are formed during a very long course of serous pleurisy (up to 20 years), when the breakdown of cellular elements containing a lot of cholesterol occurs.

Purulent tuberculous pleurisy (pyothorax, pleural empyema)

Purulent pleurisy characterized by the accumulation of purulent exudate in the interpleural gap. In addition to tuberculosis, the cause of purulent pleurisy in a patient with tuberculosis can be the lymphohematogenous spread of a pyogenic infection in various purulent and infectious diseases. Non-tuberculous empyema in these cases can retain its character until cure or quickly turn into mixed empyema as a result of exacerbation of the tuberculous process.

Tuberculous lesion of the pleura with the formation of purulent exudate more often develops with severe progression of serous and hemorrhagic pleurisy or occurs when a cavity breaks into the pleural cavity. Tuberculous empyema can be chronic. In this case, the patient’s condition worsens, the temperature rises, chills, night sweats, shortness of breath, and weight loss appear.

Empyema is especially severe with primary caseous pleurisy and disruption of the integrity of the cavity, when bronchopleural fistulas are formed. With prolonged accumulation of a large amount of pus in the pleural cavity, a pleurothoracic fistula can also form.

Chronic empyema leads to the development of amyloidosis of internal organs. With purulent pleurisy, there are pronounced changes in the leukogram and proteinogram, and hypochromic anemia develops. Mycobacterium tuberculosis is found in purulent exudate in 90% of cases.

Differential diagnosis should be carried out in relation to:

1) pleurisy with nonspecific pneumonia;

2) pleurisy with collagenosis;

3) pleurisy of a tumor nature;

4) primary pleural cancer.

A very effective research method at present is biopsy of the parietal pleura with a needle, and a valuable diagnostic method- pleuroscopy.

Antibacterial therapy tuberculous pleurisy is the main method of treatment. IN acute period diseases indicate bed rest, good nutrition with limited carbohydrates, salt and liquid, food should be rich in proteins, fats and vitamins (especially vitamin C).

The principles of treatment of tuberculosis are presented in Chapter. 5.

Treatment effectiveness increases with the use of corticosteroid hormones in the initial phase of the disease for 3-4 weeks. During the period of resorption of pleurisy, treatment with electrophoresis with calcium preparations and breathing exercises are prescribed.

With purulent pleurisy systematic and frequent evacuation of pus with washing of the pleural cavity and administration of antibiotics into the pleural cavity is necessary. Treatment of patients with chronic tuberculous or mixed empyema is complex. If there is no effect from therapeutic methods, especially in the presence of a bronchial fistula, surgical treatment is advisable.

3.2.12. TUBERCULOSIS OF THE BRONCHUS, TRACHEA, UPPER RESPIRATORY TRACT

There are three main forms of tuberculosis of the bronchi and trachea: infiltrative; ulcerative; fistula (lymphobronchial, bronchopleural fistulas).

From complications Stenoses of varying degrees, granulations, and broncholitis should be noted.

Under the influence of treatment, clinical cure can occur without residual changes and with residual changes in the form of scars, fibrous thickenings, stenoses, etc.

Tuberculosis of the oral cavity, tonsils and tongue

Oral tuberculosis is rare. If tuberculosis occurs, it is usually localized on the gums. Oral tuberculosis manifests itself as relatively painless, often ulcerating swellings, sometimes accompanied by enlarged regional lymph nodes.

Tuberculosis infections of the oral cavity and tonsils are similar and occur in connection with the consumption of infected milk or other food infected with tuberculosis or by airborne droplets. Tuberculosis of the tonsils may not manifest itself clinically.

Tuberculosis of the tongue can be either primary or secondary with advanced pulmonary tuberculosis. TB lesions on the tongue often ulcerate and can be very painful. They respond well to chemotherapy.

Clinic.

1. The patient may have a cough and sputum for some time, since tuberculosis of the larynx and pharynx occurs with severe pulmonary tuberculosis. Weight loss and other symptoms of intoxication may also occur.

3. Ear pain.

4. Pain when swallowing, which is a sign of damage to the epiglottis. The pain may be intense.

5. In severe forms of tuberculosis, specific lesions of the tongue may ulcerate.

6. Examination may reveal ulceration of the vocal cords or other parts of the upper respiratory tract.

7. Sputum examination reveals the presence of MBT.

8. A chest x-ray for tuberculosis reveals lung damage.

Differential diagnosis. The main disease with which a differential diagnosis must first be made is cancer. Malignant laryngeal cancer is rarely painful. MBT is usually detected in sputum, but a biopsy may be necessary to diagnose the tuberculous nature of the disease. If a biopsy is not possible, specific diagnostic therapy is prescribed.

Treatment. Laryngeal tuberculosis responds well to chemotherapy. If there is significant pain that is not relieved by specific treatment, prednisolone is prescribed, if possible, to more quickly resolve the inflammatory changes.

3.2.13. RESPIRATORY TUBERCULOSIS COMBINED WITH OCCUPATIONAL DISEASES OF THE LUNG (CONIOTUBERCULOSIS)

Term "coniotuberculosis" consists of 2 words (coniosis- Greek conia or conis- dust, ashes) - dust and tuberculosis.

This group includes all forms of pulmonary tuberculosis with the simultaneous presence of dust occupational diseases: silicosis, asbestosis, etc. When formulating a diagnosis, you should first write coniotuberculosis, then give a detailed description of coniosis - anthracosis, silicosis, etc. and a detailed description of the tuberculosis process.

Coniotuberculosis belongs to a large group of pulmonary diseases - pneumoconiosis. Pneumoconiosis is caused by continuous, long-term inhalation of certain types of dust particles and can result in peribronchial fibrosis, disability, and even death.

Classification of dust occupational lung diseases

Depending on the nature of the inhaled dust, up to six types of pneumoconiosis are distinguished.

1. Silicosis- a disease caused by inhalation of dust containing free silicon dioxide (SiO 2).

2. Silicates- occur when inhaling silicate dust containing silicon dioxide in a bound state.

3. Metalloconiosis- coniosis that occurs when inhaling dust from rare earth hard and heavy alloys.

4. Carboconioses- diseases are a consequence of inhalation of carbon-containing dust.

5. Pneumoconiosis- caused by inhalation of mixed dust, including those containing free silicon dioxide.

6. Pneumoconiosis- occur when inhaling organic dust (cotton, grain, cork, reed coniosis).

Pneumoconiosis have a similar pattern of changes in the lungs. The most characteristic picture is given by silicosis. However, there are no distinctive features between one and the other type of pneumoconiosis. Pneumoconiosis formations can be detected in the lung using microscopic examination. Thus, the specific cause of pneumoconiosis can be determined using specific diagnostic methods. Using the example of silicone

Brief information about the pathogenesis, clinical picture and diagnosis of pneumoconiosis is presented.

The most common cause of silicosis is quartz, making any dust harmful depending on the amount of quartz it contains.

Only the smallest quartz particles, 10 microns in size or less, are capable of causing disease.

The most common complication of silicosis is tuberculosis - silicotuberculosis. Epidemiology.

Tuberculosis is one of the important mortality factors in patients with silicosis. With the same radiological manifestations of silicosis, the risk of death is higher in patients with tuberculosis.

Epidemiological and experimental Evidence suggests that exposure to silica-containing dust, even in the absence of radiological evidence of silicosis, is a factor in the increased prevalence of pulmonary tuberculosis.

Pathogenesis. Several pathogenetic processes are common to tuberculosis and silicosis, jointly participating in the accelerated development of fibrosis and in increasing susceptibility to mycobacterial infection or reactivation of the site of latent infection. Quartz particles are phagocytosed by alveolar macrophages. Inside these cells, quartz particles are exposed to phagolysosomes. Quartz has the ability to damage the cell membrane, leading to the death of the macrophage and the release of released particles into other macrophages.

Humoral and cell-mediated immune responses are hypothesized to be suppressed by silicosis. Indirect cellular immunity- an important factor in suppressing the proliferation of mycobacteria. Fibrosis of the lung tissue, which develops in tuberculosis and silicosis, leads to impaired removal of macrophages containing dust particles or mycobacteria from the lungs. Disruption of the lymphatic system contributes to the accumulation of macrophages in the intermediate tissue of the lungs.

If the process continues, small round nodules or tangles of collagen appear in the lungs, forming along

lymphatic pathways. As the disease progresses, these distinct structures give way to large patchy areas of fibrosis or collagen accumulations throughout all areas of the lungs. Large accumulations of collagen are found in the upper parts of the lower lobes of the lungs.

Clinic. Manifestations of tuberculosis in patients with silicosis do not have any particularities. Since increased fatigue, shortness of breath, and night sweats are observed with silicosis, detection of clinical manifestations of associated tuberculosis is difficult.

Diagnostics. Focal, disseminated tuberculosis and tuberculoma are most often combined with silicosis. Diagnosis active tuberculosis in patients with silicosis requires high alertness.

The presence of tuberculosis in a patient with silicosis should be suspected in cases where radiological changes are noted in the apical regions of both lungs. These manifestations are characterized by poorly demarcated infiltrates of various sizes that do not cross the boundaries of the lung lobes. Consolidations of lung tissue may surround pre-existing silicotic lesions. The presence of cavities in the area of ​​silicotic changes is a sign of tuberculosis. The formation of cavities in the absence of tuberculosis is so rare that, from a practical point of view, any evidence of lung destruction can be taken as a sign of tuberculosis.

Signs indicating the possible presence of tuberculosis in patients with silicosis:

1) location of pulmonary pathology in the upper parts of the lungs;

2) the presence of decay;

3) relatively fast dynamics of the process;

4) the presence of pleural effusion.

Establishing a diagnosis of pulmonary tuberculosis in a patient with silicosis using bacteriological methods is difficult. Therefore, regular microscopy for the presence of acid-fast mycobacteria in sputum is recommended.

Treatment. There are no fundamental differences in the treatment of coniotuberculosis and tuberculosis. Tuberculosis associated with silicosis is recommended to be treated with standard regimens (see Chapter 5).

Prevention. Since tuberculosis is very common among patients with silicosis, anti-tuberculosis chemoprophylaxis is indicated for them.

Any complications, such as tuberculosis, emphysema, spontaneous pneumothorax or cardiac dilatation, give a very unfavorable prognosis for patients with silicosis.

3.2.14. RUSSIAN CLINICAL CLASSIFICATION OF TUBERCULOSIS AND CODES (ICD-10)

Most countries in the world use the International Statistical System for Diseases and Problems, Tenth Revision (ICD-10), approved by the World Health Organization (WHO).

The basis of ICD-10 is an alphanumeric code for coding diseases, in which the first character is indicated by a letter, and the next three by numbers. The letter denotes classes (there are 21 of them in ICD-10), the first two digits indicate the block. For greater detail, a fourth character has been introduced - a number after the dot.

The use of ICD-10 ensures the unity of information collection and comparability of materials on public health, the prevalence of diseases and their epidemiology both within one country and across different countries peace. ICD-10 makes it possible to convert verbal formulations of diagnoses into alphanumeric codes that provide computer storage and accumulation of information. The use of ICD-10 creates conditions for the automation of information about human health. This allows for comprehensive, in-depth comparative analysis data, including assessing the quality of health care in various regions of the country and the completeness of information collection.

A15-A16 Tuberculosis of the respiratory system.

A15 Tuberculosis of the respiratory system, confirmed bacteriologically and histologically.

A16 Tuberculosis of the respiratory system, not confirmed bacteriologically or histologically.

A17 Tuberculosis of the nervous system.

A18 Tuberculosis of other organs and systems (extrapulmonary localizations of tuberculosis).

A19 Miliary tuberculosis.

The Tuberculosis block includes infections caused by M. tuberculosis infiltrative M. bovis. Congenital tuberculosis (P37.0), pneumoconiosis associated with tuberculosis (J65), and consequences of tuberculosis (B90) are excluded from the “Tuberculosis” block.

The clinical classification of tuberculosis in Russia largely does not correspond to ICD-10. At the same time, the classification used in our country quite fully, at least at present, satisfies the requirements of phthisiatricians in Russia. In this regard, the adaptation of the domestic classification of tuberculosis to ICD-10 and the development of an adapted coding version that meets both the requirements of the international classification and domestic phthisiology are very important.

Is the Russian clinical classification of tuberculosis approved by order of the Russian Ministry of Health? 109 of March 22, 2003

Tables 3-1 and 3-2 of this section present the clinical classification of tuberculosis currently used and the codes recommended for encoding diseases according to ICD-10. Some provisions of this classification may be revised in subsequent years. In accordance with this, the code signs will also be changed. To accurately record patients with different localizations of tuberculosis when establishing a diagnosis marked with a special sign (f), additional coding is required for a different class of disease.

ICD-10 does not provide for the coding of a number of essential signs that Russian TB specialists use when diagnosing tuberculosis and determining patient management tactics. In this regard, it is proposed to use additional characters to encode some of the most important features (Table 3-3). To indicate the corresponding signs in the domestic clinical classification of tuberculosis in accordance with the ICD-10 code, code dictionaries have been developed.

Table 3-1. Main clinical forms of tuberculosis

Note. If a term has a dual classification (according to the etiology and manifestation of the disease), both codes are given: the first is followed by a special sign (t), and the second by an asterisk (*).

Table 3-2. Residual changes after cured tuberculosis

Table 3-3. Characteristics of additional signs

Metatuberculous changes in the lungs in most cases occur after a history of lung disease. Most often these are consequences of tuberculosis, although there are cases of similar consequences after other pulmonary diseases.

Changes in the lungs are usually detected by a radiologist during a routine medical examination. Metatuberculous (meta - after suffering) changes are spoken of as an x-ray term, although in fact the changes can be life-threatening.

Note that the changes under consideration are not oncological. However, if you find any questionable changes, it's worth checking.

Tuberculosis is an infectious disease caused by an acid-fast bacterium called Koch bacillus. Tuberculosis can affect all organs and tissues, but most often it is localized in the lungs. This disease does not go away without a trace. Changes always remain, which are called metatuberculous foci.

Metatuberculosis is the name given to foci of connective tissue proliferation or calcium deposits in the area where tuberculosis was suspected to have existed before. They can be seen using a survey x-ray.

For reference. The very concept of “metatuberculosis” means that the picture seen is a residual sign of previous tuberculosis. In fact, connective tissue can appear as a result of any inflammation that ends in necrosis. The etiology of this inflammation is difficult to determine, because not every proliferation of connective tissue can be called metatuberculosis.

In the classical sense, metatuberculosis is any change that remains after tuberculosis in its active or latent form. Other cases of proliferation of connective tissue in the lungs should be called pneumosclerosis or pneumofibrosis.

Metatuberculous changes in the lungs - what is it?

The lungs are the “favorite organ” of Koch’s rods. Mycobacterium tuberculosis is aerobe, and therefore is more often found in well-ventilated areas - the upper lobes of the lungs. Meatuberculosis foci are most often localized here.

Any residual phenomenon that occurs due to the activity of Koch's bacillus can be called metatuberculosis. For example, Gon's lesion is a metatuberculous change that arose after primary tuberculosis. It is localized, most often, in the upper lobes of the lungs. Any focus localized in this place should raise suspicion of tuberculosis or its residual effects.

Such changes can be seen using radiography. On film they appear as darkened areas (light) against the background of normal (black) lung tissue, which indicates the presence of connective tissue in the lungs.

Metatuberculous changes in the lungs can be distinguished from other types of pneumosclerosis using several signs:

• It is known for sure that there was tuberculosis in this place previously;
• Localization in the upper lobes of the lungs;
• Retrospectively, symptoms indicating previous tuberculosis were identified (cough, fever, hemoptysis);
• Other possible causes of connective tissue have not been identified.

Types of metatuberculous changes

Like any pathological change in lung tissue, metatuberculosis can be local and diffuse. In the first case, one or several lesions are visible, small in size, clearly demarcated from healthy lung tissue. Such changes occur due to focal or infiltrative tuberculosis.

Diffuse changes are characterized by extensive proliferation of connective tissue, which makes it difficult to distinguish the shadow of a healthy lung. At the same time, the lung decreases in size and breathing becomes difficult.

Depending on what is in the pathological focus, there are two types:

• cirrhotic meatuberculosis,
• calcifications.

Cirrhotic metatuberculosis

Cirrhosis is the proliferation of connective tissue as a result of the inflammatory process. With such metatuberculosis, connective tissue appears in areas where there was previously caseous necrosis.

Soon it fills all the areas where the lung was destroyed. This may be one or several lesions, as well as an entire lobe or even the entire lung. The more pronounced the cirrhosis, the more symptoms of metatuberculosis.

For reference. As a rule, after tuberculosis there are always foci of cirrhosis varying degrees expressiveness.

Calcifications in the lungs

In this pathological condition, calcium salts begin to be deposited in the place where there was previously inflammation. This microelement is constantly present in the blood and cells of all organs; it is necessary for their normal functioning.

For reference. At the site of inflammation, the amount of calcium often increases, and after the inflammatory process subsides, salts of this element are formed. They are deposited in the form of crystals.

Often such lesions are visible against the background of overgrown connective tissue, but sometimes they are found without it. On x-rays, calcifications appear as white areas, similar in density to bone.

In addition, any type of metatuberculosis can be stable or progressive. In the first case, the resulting lesions are not prone to growth; they do not increase in number or size. In the second case, the pathological process tends to progress, affecting increasingly larger areas of healthy tissue.

Symptoms of metatuberculosis

Manifestations of this pathological condition depend on how much lung tissue is affected. If there is one
a small lesion of connective tissue or small calcifications, there may be no symptoms.

With extensive lesions, the patient experiences respiratory failure and other complications, which manifest themselves as follows:

• Shortness of breath that occurs when inhaling or exhaling;
• Dry cough;
• Pale skin, bluish nasolabial triangle and fingertips;
• Fingers in the form of drumsticks (with thickening of the nail phalanges);
• Fatigue, constant feeling of tiredness;
• Asymmetry of the chest, reduction of one of its halves.
• Pain in the chest (with damage to the pleura).

For reference. These symptoms develop gradually. Cough and shortness of breath may appear as soon as the connective tissue begins to compress the bronchial tree.

Asymmetry of the chest occurs in the case of the development of extensive atelectasis (collapse of the lung or part of it). A change in skin color occurs if the surface area for gas exchange in the lungs decreases significantly.

This also causes deformation of the fingers, but several years must pass for the development of “drumsticks”. Pain only says that pathological changes affected the pleura, there are no pain receptors in the lungs themselves.

The essence of the changes

During the height of tuberculosis, mycobacteria destroy lung tissue or other body structures. Such lesions are called caseous necrosis. Dead lung tissue cannot regenerate, but the place where it was located does not remain empty. Here connective tissue or calcifications form, such a change is called metatuberculosis.

Important. The larger the initial lesion, the more connective tissue will remain, but it will not completely correspond to the shape and volume of the tuberculosis lesion. The connective tissue tightens the lung, compresses the bronchi, and blocks their lumen. In addition, it is not capable of gas exchange and has much fewer vessels.

All this leads to respiratory failure and increased stress on the heart. Such pathological processes are observed only in patients with extensive forms of tuberculosis. If the lesions are small, they are discovered by chance during the next medical examination.

Between connective tissue Sometimes calcium salts are deposited, which is clearly visible on chest radiography. In disseminated and miliary forms of tuberculosis, calcifications can be located in small foci and without connective tissue. Calcium salts themselves do not cause any complications.

At-risk groups

Metatuberculosis can only develop in those who have had tuberculosis, therefore the risk groups for these diseases are the same. First of all, these are people with reduced immunity and people who often encounter aggressive strains of Koch's bacillus.

These factors weaken the body, contribute to the development of extensive changes in the lungs, which significantly affect the state of health even after subsiding active process.

Risk groups for developing metatuberculous changes in the lungs include:

• Patients with acquired or congenital immunodeficiency;
• Prison prisoners;
• TB doctors;
• Forensic laboratory workers;
• Children and adults who are often and long-term ill;
• Patients with diabetes;
• Persons who abuse alcohol;
• People with disabilities eating behavior(anorexia, bulimia).

Attention. It is worth remembering that tuberculosis, as well as its consequences, can develop in any person, regardless of social status and type of activity.

Treatment

Metatuberculous changes in the lungs, like any other residual effects, cannot be cured. There are no drugs that can transform connective tissue or calcium salts into normal lung.

Important. Only those lesions that contain not only connective tissue, but also active Koch bacilli are subject to treatment.

In this case, the patient can cough up mycobacteria, becoming re-infected himself and infecting others. In this case, surgical excision of all metatuberculous foci is indicated.

Complicated metatuberculosis is treated symptomatically. For this purpose, drugs are prescribed that help improve blood supply to the lungs, facilitate the work of the heart, as well as expectorants, antitussives and painkillers. medicines.

For reference. The main therapy should be aimed at preventing the worsening of the existing condition, which is only possible with lifestyle changes.

Prevention of complications in metatuberculosis pathologies

Complications of metatuberculosis can be both from the lungs and from the heart. The first group includes respiratory failure, atelectasis (collapsed lung or airlessness of the lung tissue - a dangerous disease) and emphysema (hyper airiness). The second group includes heart failure, increased pressure in the pulmonary circulation and acquired heart defects.

In order to prevent the development of these conditions, it is necessary to adhere to recommendations for lifestyle changes. Most often, the patient is given the following advice:

• Quitting smoking and alcohol;
• Daily walks fresh air;
• Compliance with work and rest, sleep and wakefulness;
• Daily performance of gymnastic exercises;
• Mastering the special breathing of yogis;
• Balanced nutrition, increased consumption of proteins and vitamins;
• Treatment of concomitant pathologies;
• Completing courses of sanatorium-resort treatment.

Forecast

Important. The prognosis of this pathology can be called doubtful. Metatuberculous changes in the patient’s lungs will remain in any case; their reverse development is impossible.

However, it is possible to prevent the occurrence of complications or stop the process of their development. In this case, metatuberculosis can exist in the patient’s lungs for a very long time without symptoms.

In the best case scenario, small foci of metatuberculosis will not affect the patient’s life in any way. In the most unfavorable case, death is possible due to respiratory or heart failure.

Residual changes in the lungs after recovery from tuberculosis

As a result of treatment, complete and traceless disappearance of tuberculosis tubercles may occur, which is accompanied by negative tuberculin reactions. This outcome is possible with a disease of short duration, with so-called fresh processes that occur without extensive caseous necrosis in the center of inflammation. These forms of true healing are quite rare. In the majority of patients (95-96%), cure is associated with the obligatory development of residual changes in the lung tissue.

Residual changes should be understood as various formations in the lung tissue that persist at the time of clinical cure in individuals receiving antibacterial drugs, as well as during spontaneous cure of the tuberculosis process.

It is necessary to distinguish between small residual changes in the lungs and pleura: slight fibrosis, cicatricial changes, single petrifications less than 1 cm in diameter, single, clearly defined foci, pleural layers and large residual changes: severe pneumosclerosis, single or multiple petrifications with a diameter of 1 cm or more, multiple clearly defined foci against the background of pneumosclerosis, large long-existing dense foci, cirrhosis (carnification of the lung with its cirrhotic transformation), the formation of extensive pleural adhesions.

Particular attention is paid to the issue of completing the treatment of cavities (cleaned, sanitized cavities). The cavity can take on a cystic shape, but a “sanitized” cavity, especially with fibrocavernous tuberculosis, does not mean a lasting recovery. After chemotherapy is stopped, the process may progress.

The difference in residual changes in size and extent, in the nature of the anatomical and histological structures, largely determines the possibility of reactivation of the tuberculosis process. Persons under observation in the VII group of dispensary registration are currently one of the main sources of replenishment of the contingents of patients with active forms of pulmonary tuberculosis. This is due to endogenous reactivation of tuberculosis.

Current task modern therapy tuberculosis is to improve treatment methods to achieve clinical cure with minimal residual changes. Long-term complex antibacterial therapy leads to the formation of minimal residual changes and more complete types of healing, further reducing the possible risk of relapse of tuberculosis.

The best result is achieved with a fresh and timely identified focal process. Fresh lesions completely disappear, perifocal inflammation is eliminated around older lesions; Fibrous changes and encapsulated lesions are worse or do not undergo reverse development at all.

Residual changes in the form of single foci against the background of cicatricial changes and multiple foci are observed in patients in whom the process was of a certain duration and was very widespread.

In infiltrative-pneumonic pulmonary tuberculosis, the most common residual changes are foci of compaction and fibrosis. More rapid and complete resorption of tuberculous infiltrate is observed in patients with drug-sensitive mycobacterium tuberculosis compared with patients who secrete predominantly resistant strains of mycobacteria. Pulmonary tuberculomas are characterized by a long course of the tuberculosis process, which is determined by the stability of changes in the lung tissue.

In fibrous-cavernous pulmonary tuberculosis, complete resorption of pathomorphological changes is not observed. The formation of single lesions against the background of moderate inductive changes is possible. When fibrous-cavernous pulmonary tuberculosis is cured, residual changes are pronounced with a predominance of the phenomena of pneumosclerosis and fibrosis.

After effective antibacterial therapy has been completed, the involution of residual changes continues for a certain time. The specific changes remaining in the lung tissue continue to decrease, despite the cessation of direct exposure to antibacterial drugs, which is due to favorable immunobiological changes in the body under the influence of the treatment, causing an increase in general and local tissue resistance. In specific foci, the cellular composition changes, the processes of fibrosis and hyalinosis increase, the remaining areas of caseous necrosis continue to partially resolve, become delimited and thicken until calcification occurs. Large focuses are reduced, indurated or turned into small ones focal formations. Even the calcification phase in some cases is not final. It is replaced by a phase of dissolution of calcium salts deposited in the lesions. The dynamics of inactive tuberculosis changes become positive over time due to the metabolic processes occurring in them, leading to dehydration and compaction. Antibacterial and restorative treatment accelerates these processes and reduces the potential activity of tuberculous changes. In this regard, repeated anti-relapse courses of antibacterial therapy play a particularly important role, which not only help prevent relapses of the tuberculosis process, but also make it possible to minimize residual changes in the lungs.

Persons in the III group of dispensary registration of patients with inactive tuberculosis of the respiratory system, depending on the size and nature of residual changes, are divided into two subgroups: with large residual changes (subgroup A) and with small residual changes (subgroup B). Persons with large residual changes in this group of dispensary observation are from 3 to 5 years, with small residual changes - up to 1 year. In case of large residual changes with the presence of aggravating factors that weaken the body's resistance, it is necessary to carry out anti-relapse treatment with tuberculostatic drugs in the spring and autumn on an outpatient basis or (if indicated) in a sanatorium. In the grouping of contingents served by anti-tuberculosis institutions, the VII group of dispensary observation was introduced in 1974. This is a group of people with an increased risk of relapse and tuberculosis disease, subgroup A of which includes people with large residual changes transferred from group III of dispensary observation, and with small residual changes in the presence of aggravating factors. They are monitored at the dispensary for life, with a mandatory annual visit to the dispensary and a full clinical and x-ray examination. They should be subject to general health measures aimed at increasing resistance to tuberculosis. In this group, it is possible to conduct courses of chemoprophylaxis when factors appear that weaken the body’s resistance.

Among infectious diseases, which lead to death, the most common is pulmonary tuberculosis and its extrapulmonary forms. The causative agent is Mycobacterium tuberculosis, which enters the body of a healthy person primarily through airborne droplets.

Further, mycobacteria, if a person’s immune forces are weakened, begin to actively multiply and spread throughout the body, affecting internal organs. If the diagnosis of tuberculosis and the main course of treatment are not carried out in a timely manner, the complications and consequences of tuberculosis may be irreversible. The patient may become disabled, and in severe cases, death from pulmonary tuberculosis occurs.

Post-tuberculosis changes significantly reduce the patient’s quality of life. Therefore, everyone affected by this terrible disease must understand how pulmonary tuberculosis is dangerous and what it leads to, how to survive it, know the features of tuberculosis treatment methods and signs of pathological abnormalities in case of complications.

The most common complications include chronic nonspecific respiratory diseases. People often talk about so-called residual changes after tuberculosis. This refers to various formations in the lung tissues, tubercles, and compactions that remained at the time of the patient’s clinical recovery. These are fibrosis, scars, (calcifications) of various sizes and shapes, which can either resolve completely over time, or lead to the development of new complications, for example, pneumothorcus (more details below).

Secondary tuberculosis

Often doctors have to deal with so-called secondary tuberculosis. That is, the focus of infection, which was considered extinct after treatment, under the influence of certain factors becomes active again and the disease develops again. The cause of secondary tuberculosis in most cases is repeated contact with active mycobacteria, a sharp decrease in immunity due to another illness, stress, injury, or poor lifestyle.

Complications of primary tuberculosis

Atelectasis

Atelectasis occurs as a complication of tuberculosis pathology if treatment was carried out incorrectly or was not completed. Due to blockage of the bronchi, part of the lung collapses. The alveoli of the lung stick together, and air does not enter the affected part of the lung. Thus, the gas exchange process is disrupted, and symptoms of respiratory failure develop.

The severity of atelectasis directly depends on which parts of the bronchi are affected. If there is a blockage of the main bronchus, then gas exchange throughout the entire part of the lung is disrupted. If the patency of the small branches of the bronchi is impaired, then only one segment of the lung collapses. Metatuberculous changes are detected with atelectasis by the following symptoms:

• chest pain;
• attacks of shortness of breath;
• increased heart rate with decreased blood pressure;
• cyanosis of the skin.

To stop further pathological changes in the tissues of the lungs, it is necessary first of all to restore the patency of the bronchi.

Pneumosclerosis

Pneumosclerosis is one of the most severe residual changes of pulmonary tuberculosis. As a rule, it develops with advanced atelectasis: ventilation of the segment of the affected lung is impaired, as a result of which the lung tissue is replaced by connective tissue. Pneumosclerosis is often discovered after surgery on the lungs, scarring of the affected tissue.

Pneumosclerosis manifests itself with the same symptoms as atelectasis. The most important thing with such a complication is to prevent secondary infection, the formation of “honeycomb lung” or heart failure.

Fistulas

Fistulas as a complication of severe tuberculosis can be bronchial or thoracic. A fistula is a pathological channel connecting several points of the respiratory organs. How clearly a fistula will manifest itself clinically depends on its diameter and anatomical location.

The presence and severity also plays a role inflammatory processes in the pleura, as well as the “age” of the fistula. Often such complications develop after surgery on the bronchi or lungs. Bronchopleural fistulas may not manifest themselves at all, or may make themselves felt only from time to time with bouts of dry cough with the release of a small amount of sputum.

Pneumothorax

This complication is considered more dangerous than the others, but it does not develop as often. It is usually caused by other respiratory diseases, in which the pleura, the inner lining of the lungs, becomes inflamed. is formed when the integrity of the pleura is violated, resulting in communication with the respiratory tract. Pneumothorax can be recognized by the following signs:

1. Sharp chest pain, preceded by sneezing, laughing, coughing, especially severe.
2. Dyspnea.
3. Attacks of weakness, cold sweat, rapid pulse, pale face.
4. Falling blood pressure, difficulty breathing.

Treatment of pneumothorax is carried out in a hospital setting; a delay in diagnosis and proper therapy can lead to the death of the patient.