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Cavernous and fibrous-cavernous pulmonary tuberculosis

 
, medical expert
Last reviewed: 23.04.2024
 
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With a relatively favorable flow of tuberculosis, infiltration and fresh foci sometimes dissipate quickly, but the cavity of decay in the lung tissue can be preserved, delimited and transformed into a cavern. Under conditions of specific chemotherapy, this process became much more frequent, and cavernous tuberculosis was isolated in a separate clinical form. Tubercular cavern is a cavity formed in the zone of tubercular lesion, delimited from the contiguous pulmonary tissue by a three-layered wall.

After the formation of the cavern, the original form of tuberculosis loses its typical manifestations, and the tubercular process, which remains active, acquires new features. An important feature of cavernous tuberculosis is the limited and reversible nature of morphological changes, manifested as a thin-walled cavity without pronounced infiltrative, focal and fibrous changes in the adjacent pulmonary tissue.

The cavern is a constant source of infection and threatens the progression of the tuberculosis process with its transformation into fibro-cavernous pulmonary tuberculosis. The development of fibro-cavernous tuberculosis can be prevented by the timely appointment and consistent implementation of a set of adequate medical measures.

Fibrous-cavernous tuberculosis is characterized by the presence of one or more caverns with a well-formed fibrous layer in the walls, expressed by fibrous and polymorphic focal changes in the lung tissue.

For fibro-cavernous tuberculosis, a typical wavy, usually progressive course is typical. At the same time, severe specific lesion of pulmonary tissue with coarse fibrosis limits the possibilities of effective therapeutic influence on the pathological process.

There are three main variants of fibrous-cavernous tuberculosis:

  • limited and relatively stable;
  • progressive:
  • complicated.

trusted-source[1], [2], [3], [4], [5]

Epidemiology of cavernous and fibrous-cavernous pulmonary tuberculosis

Cavernous and fibrous-cavernous tuberculosis of the lungs is mainly caused by adults. In children with primary forms of tuberculosis: the primary tuberculosis complex and tuberculosis of the intrathoracic lymph nodes - the formation of caverns is rarely observed.

Cavicular and fibrous-cavernous tuberculosis is diagnosed in 3% of newly diagnosed patients (of which cavernous is not more than 0.4%). Among patients observed for active tuberculosis in dispensaries, cavernous tuberculosis occurs in about 1%, fibro-cavernous tuberculosis occurs in 8-10%.

Fibrous-cavernous tuberculosis and its complications are the main cause of death of patients with pulmonary tuberculosis. Among patients who died of tuberculosis, fibro-cavernous tuberculosis was in 80%.

trusted-source[6], [7], [8]

Pathogenesis of cavernous and fibrous-cavernous pulmonary tuberculosis

Disintegration of the lung tissue with the subsequent formation of the cavity is possible with the progression of any form of pulmonary tuberculosis. This is facilitated by a decrease in general and immunological resistance against additional sensitization. Massive superinfection, attachment of various diseases, drug resistance of mycobacteria.

Impaired immunity and the inevitable increase in the number of bacterial population in this case are accompanied by increased exudation, the development of microcirculatory disorders and damage to the surfactant system. The destroyed cellular elements form caseous masses filling the alveoli. Under the action of proteolytic enzymes released by leukocytes, the caseous masses melt and undergo partial resorption by macrophages. When rejecting caseous masses through the drainage bronchus, a pneumonogenic decay cavity is formed. In other cases, the destructive process can begin with the defeat of the bronchus and the development of panbronchitis with the subsequent destruction of the adjacent pulmonary tissue and the formation of a bronchogenic cavity of decay. Another way of formation of the bronchogenic cavity is the penetration of the pathogen into the previously formed bronchiectasis.

The decay cavity is immediately surrounded by a wide layer of caseo-necrotic masses. Outside, tubercle granulations, mainly formed by epithelioid and giant cells, adhere to them. Over time, collagen fibers form in the outer part of the granulation layer, which form a thin fibrous layer with a non-uniform structure. As a result, around the cavity appears three-layer wall, characteristic for the cavity. The inner layer of the wall forms caseous-necrotic masses, the middle is represented by a granulation tissue, the outer one by concentrically arranged fibrous fibers. The formation of the wall of the cavity usually takes several months. Exceptions are due to the rejection of caseo-necrotic masses from the encapsulated focus (tuberculosis). In this case, a cavity appears with a three-layered wall, in which a previously formed fibrous layer already exists.

The fresh (early, sharp) cavern has a round or oval shape, is surrounded by a small-change pulmonary tissue without significant inflammatory and fibrotic changes. Such a cavity is typical for cavernous tuberculosis of the lungs.

Depending on the nature and the specific mechanism of formation, proteolytic, sequestering, alterative and atheromatous caverns are isolated. In cases where melting of caseous masses begins at the center of the pneumonic focus and gradually spreads to the periphery, a proteolytic cavity is diagnosed. The melting of caseous masses in the marginal regions with the advance towards the center of the caseous focus is a sign of a sequestering cavity. At melting of caseous masses in the encapsulated foci, atheromatous cavities arise. Sometimes the main cause of the decay are disorders of microcirculation and nutrition of tissues in the area of tubercular lesion, followed by necrosis of individual sites. Such a mechanism of formation is characteristic of an alterative cavity.

In connection with the formation of a cavern, tubercular inflammation, as a rule, extends to the mucosa of the draining bronchus. Tubercular granulation narrowed its lumen and made it difficult to move air from the cavity. As a result, its volume can increase significantly, and the cavern becomes "bloated." Deterioration of bronchial drainage complicates the evacuation of the contents of the cavity, increases the inflammatory response and general intoxication.

On the background of treatment, the following options for the involution of a fresh cavern are possible:

  • rejection of caseo-necrotic masses, transformation of the granulation layer into fibrous and healing of the cavity with scar formation. This is the most perfect variant of cavern healing;
  • filling the cavity with a granulation tissue and lymph that partially dissolve, and then germinate with a connective tissue. The result is a focus or focus;
  • when tubercular inflammation is eliminated in the drainage bronchus and its scarring obliteration, the air from the cavity is absorbed and it falls off. Conditions are created for reparative processes and the formation of a focus or focus in the place of the cavern;
  • with the preservation of the normal structure and function of the draining bronchus, a gradual epithelization of the internal wall of the cavity occurs. However, the epithelium, which grows out of the bronchus, does not always line the cavern completely. This option of healing is not completely reliable;
  • it is possible to combine different ways of cavity involution.

With the progression of cavernous tuberculosis, caseo-necrotic inflammation spreads beyond the walls of the cavity, develops caseous lymphangitis and endobronchitis, and fresh foci of specific inflammation form in the pericavitic zone. Bronchogenic dissemination of mycobacteria determines the formation of tuberculous foci and foci in previously unaffected lungs. The fibrous layer of the cavity wall gradually becomes thicker and denser, fibrous changes develop in the adjacent lung tissue. The wall of the cavity is deformed, the shape of the cavity becomes irregular.

Over time, the outer fibrous layer of the cavity wall becomes thick and continuous. The inner surface of the cavity wall is often uneven, a small amount of mucopurulent contents with crumbs of caseous masses may be present in the cavity. Such cavern is called fibrous or old. Its formation testifies to the transformation of cavernous tuberculosis into fibro-cavernous tuberculosis of the lungs.

First, fibrous-cavernous tuberculosis may have a relatively limited extent and not show a clear tendency toward progression (limited and relatively stable fibrous-cavernous tuberculosis). In the future, the size of the fibrous cavity increases, the partitions between closely located caverns are destroyed and multi-chambered, often giant tubercular caverns are formed. In the septa separating the cavity, there are blood vessels, and their destruction often leads to pulmonary hemorrhage. The centers of bronchogenic seeding in the lungs tend to merge into foci with the gradual formation of new caverns. Over time, in the walls of caverns, lung tissue and pleura, severe destructive, fibrous and degenerative changes are formed that are irreversible. As a result of deformation and destruction of the bronchi, cylindrical and saccular bronchiectasis are formed, which are often filled with purulent contents. The branches of the pulmonary artery narrow and partially obliterate, and the bronchial arteries expand, especially near the walls of the caverns. This clinical form is designated as a common progressive fibrous-cavernous pulmonary tuberculosis. In this form, empyema of the pleura and tubercular lesions of other organs are often found, in particular, sputogenic tuberculosis of the larynx or intestine. Fibrous-cavernous tuberculosis can be accompanied by amyloidosis of the kidneys, liver, spleen. The complicated course of fibrous-cavernous tuberculosis with the development of caseous pneumonia often leads to a lethal outcome.

Symptoms of cavernous and fibrous-cavernous pulmonary tuberculosis

Cavernous tuberculosis of the lungs is more likely to develop on the background of insufficiently successful treatment of other forms of tuberculosis. Patients may be disturbed by a cough with a small amount of mucous sputum: sometimes they note increased fatigue, decreased appetite, unstable mood. Such complaints are often updated with a considerable duration of the previous treatment and a large drug load. In patients with newly diagnosed cavernous tuberculosis, complaints, as a rule, are absent. When percussion of the chest over the region of the cavity, one can determine the shortening of the percussion sound due to the compaction of the pleura and the pulmonary tissue around the cavity. After coughing and deep inhalation over the affected area, sometimes a few wet and dry rales are heard. In most patients, the caverns are "dumb", i.e. They are not detected using physical methods of investigation.

For patients with fibro-cavernous pulmonary tuberculosis, symptoms of intoxication, cough with sputum, sometimes with a trace of blood, dyspnea are characteristic. They can reveal the deformation of the chest, the displacement of the mediastinal organs towards the lesion, expressed and diverse stoacoacoustic symptoms. The severity of the clinical manifestations of fibrous-cavernous tuberculosis changes in waveform depending on the phase of the tuberculosis process: the abundance of complaints during exacerbation and the relatively satisfactory state in the period of short-term remissions.

Adequate treatment of fibro-cavernous tuberculosis in most patients contributes to the stabilization and delimitation of the lesion. As a result of long-term treatment, pericavitic inflammation decreases, the granulation layer is partially sanitized, tubercular foci dissolve. Such dynamics are more often observed with limited fibrous-cavernous tuberculosis.

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X-ray picture of cavernous and fibrous-cavernous pulmonary tuberculosis

In the X-ray study, tubercular caverns are more often found in the upper parts of the lungs, where the decay cavities are localized in many clinical forms preceding the development of cavernous tuberculosis. The most informative method for diagnosing caverns and accompanying changes in lungs is CT.

With cavernous tuberculosis, one cavern of round shape is usually detected no more than 4 cm in diameter. The thickness of the cavity wall is 2-3 mm. The inner contour of the wall is clear, the outer is more often uneven and blurred, especially with persistent perifocal inflammation. When forming a cavern from focal tuberculosis or tuberculoma, changes in the surrounding pulmonary tissue are insignificant. The shadows of fibrous scars and foci are more often detected around caverns that have developed from infiltrative or disseminated pulmonary tuberculosis. The cicatricial cavity has an irregular shape with strands to the root of the lung and pleura.

With fibro-cavernous tuberculosis of the lungs, the radiographic picture is diverse and depends on the initial form of tuberculosis, the prescription of the disease, the prevalence of the lesion and its characteristics. One or several ring-shaped shadows are detected, a fibrous decrease in the affected parts of the lung, polymorphous focal shadows of bronchogenic colonization. The diameter of the ring-shaped shadows varies from 2-4 cm to the size of the lobe of the lung, the shape can be round, but more often it is irregular or polycyclic (when several caverns are combined). The outline of the inner contour of the cavity wall is sharp, the outer contour on the background of compacted pulmonary tissue is less clear. Sometimes in the lumen caverns determine the sequestration or liquid level.

In the upper-lobe localization of the cavern in the lower parts of the lungs, polymorphic foci and foci of bronchogenic colonization are found. In the lesion zone there is a local or diffuse fibrous tightness with areas of increased transparency. A decrease in the volume of the affected lung leads to a shift in the mediastinal organs towards the lesion. The intercostal spaces narrow, the dome of the diaphragm rises. In the middle and lower parts of both lungs are visible foci of bronchogenic seeding, which, when progressing, turn into foci and cavity decay.

With bilateral fibrous-cavernous tuberculosis, formed from a hematogenous disseminated cavern, and fibrotic changes are localized in the upper parts of the lungs rather symmetrically. In the lower sections, the transparency of the pulmonary fields is increased.

In the process of treatment of fibro-cavernous tuberculosis, positive resorption is considered a resorption of infiltrative and focal changes in the lungs, a decrease in the thickness of the cavity wall. However, usually caverns remain and are well visualized by X-ray and CT.

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