Disseminated pulmonary tuberculosis: what is happening?

Disseminated pulmonary tuberculosis can develop with a complicated course of primary tuberculosis as a result of increased inflammatory response and early generalization of the process. More often disseminated tuberculosis occurs several years after the clinical cure of primary tuberculosis and the formation of residual post-tuberculosis changes: the focus of the Gon and / or calcinate. In these cases, the development of disseminated tuberculosis is associated with late generalization of the tuberculosis process.

The main sources of dissemination of mycobacteria in the development of disseminated tuberculosis are the residual foci of infection in the intrathoracic lymph nodes, which are formed during the reverse development of the primary period of tuberculosis infection. Sometimes the source of dissemination of mycobacteria in the form of a calcified primary focus can be localized in the lung or other organ.

The causative agent can spread through the body in various ways, but most often the dissemination occurs with the blood flow. The hematogenous pathway underlies about 90% of all disseminated lesions in tuberculosis.

The likelihood of developing disseminated pulmonary tuberculosis increases with the influence of factors that weaken the human immune system, with prolonged and close contact with bacteriovirus.

Depending on the path of mycobacterial distribution and the location of tuberculosis foci along the course of blood and / or lymphatic vessels, disseminated pulmonary tuberculosis can be hematogenous, lymphogenous and lymphogenic.

A mandatory condition for the development of hematogenous disseminated tuberculosis is considered bacteremia. However, the increased sensitivity of cells and tissues to mycobacteria and changes in the functional state of the nervous and vascular systems are also important for the onset of the disease. Violation of cortico-visceral regulation leads to vegetative-vascular dystonia and microcirculatory disorders. Blood flow in small vessels slows down, and the causative agent penetrates through the vascular wall into the adjacent tissue. The increased sensitivity of cells to mycobacteria, formed in the initial period of tuberculosis infection, ensures rapid absorption of mycobacteria by macrophages, which then lose the ability to move and settle in the perivascular tissue. Further movement of the pathogen is suspended, but the destruction of mycobacteria is difficult and even impossible due to a decrease in the bactericidal potential of macrophages. As a result, many tuberculosis foci are formed in the interstitial tissue of the lungs along the course of the vascular-bronchial bundles. With hematogenous distribution of mycobacteria, foci are found in both lungs relatively symmetrically.

Lymphogenous dissemination in the lungs occurs when the mycobacteria are distributed with retrograde lymph flow. The appearance of the process is due to the reactivation of inflammation in the intrathoracic lymph nodes and the development of lymphostasis. Lymphogenous distribution of mycobacteria often leads to unilateral dissemination and mainly radical localization of foci. There is also a bilateral lymphogenous dissemination. From the hematogenous it is distinguished by the asymmetric location of the foci in the lungs.

The nature of the inflammatory reaction and the prevalence of foci in disseminated tuberculosis are due to the individual reactivity of the organism, the massiveness of bacteremia, and the severity of immunological and functional disorders. The size of the foci largely depends on the caliber of vessels involved in the pathological process.

According to pathomorphological studies, three variants of disseminated pulmonary tuberculosis are distinguished. They correspond to the clinical features of its course: acute, subacute and chronic.

[1], [2], [3], [4], [5], [6], [7], [8]

Acute disseminated pulmonary tuberculosis

Acute disseminated pulmonary tuberculosis occurs with a significant decrease in anti-tuberculosis immunity and massive bacteremia. Hyperergic reaction of the pulmonary capillaries to bacterial aggression with a significant increase in the permeability of their walls creates favorable conditions for the penetration of mycobacteria into the alveolar septa and alveolar walls. In the course of the capillaries, multiple, uniform, prosovoid (from the Latin "milium" - millet) and yellowish-gray foci appear almost simultaneously. They protrude above the surface of the lung slice in the form of tubercles 1-2 mm in diameter and are localized evenly in both lungs. Edema and cellular infiltration of interalveolar septa significantly reduce the elasticity of the lung tissue. Exudative or cheesy-necrotic reaction very quickly replaces the productive, so the fusion of foci does not occur. This form of acute disseminated tuberculosis is called miliary.

Sometimes the generalization of the tuberculosis process is observed: multiple caseous foci with a large number of mycobacteria are found in other organs (tuberculosis sepsis).

With timely diagnosis and full treatment, the miliary foci can almost completely resolve. Simultaneously, signs of emphysema disappear and the elasticity of the pulmonary tissue is restored.

[9], [10], [11], [12], [13], [14], [15], [16]

Subacute disseminated tuberculosis of the lungs

Subacute disseminated pulmonary tuberculosis develops with less gross violations in immunity and less massive bacteremia. Intralobular veins and interlobular branches of the pulmonary artery are involved in the pathological process. The foci formed around the venules and arterioles have medium and large sizes (5-10 mm), often merge, forming conglomerates in which destruction can occur. The inflammatory reaction in the foci gradually becomes productive. In the walls of the alveoli and interalveolar septa develop productive obliterating vasculitis and lymphangitis, in the pulmonary tissue around the foci appear signs of emphysema.

With subacute disseminated tuberculosis of strict symmetry, lung damage is not noted. Foci are more often found in the upper and middle parts, mostly subpleural. Dissemination is not limited to the lungs and often extends to the visceral pleura. Often the upper respiratory tract, especially the outer ring of the larynx, is involved in the process.

Specific therapy promotes resorption and compaction of foci. Complete resorption of the foci is rarely observed. There are fibrotic and atrophic changes in the interalveolar septa. Emphysema, formed in the initial period of the disease, becomes irreversible.

Chronic disseminated tuberculosis of the lungs

Chronic disseminated pulmonary tuberculosis usually develops slowly as a result of repeated waves of lymphohematogenous dissemination, which are not diagnosed in a timely manner. At the next wave of dissemination, fresh foci appear in intact parts of the lung, where blood flow was not disturbed at the beginning of the disease. Repeated waves of dissemination cause a "floor" location of the foci in both lungs. First foci can be found in the apical and posterior segments. The greatest number of foci are found in the upper and middle parts of the lungs. They are localized predominantly subpleural. On the surface of the lung incision, a thin loop net of whitish-gray fibrous strands is clearly visible, associated with diffuse perivascular and peribronchial fibrosis. Sometimes you can find massive scars in the lung tissue and pleural fibrosis, which indicate a significant prescription of the tuberculosis process. Fibrotic changes are more pronounced in the upper parts of the lungs, and in the lower parts can be observed the development of vicarious emphysema.

Between the foci formed at different times, there are significant morphological differences. In the fresh foci, a pronounced productive tissue reaction predominates. The foci, having a great prescription, are surrounded by a capsule. The old foci are partially replaced by a fibrous tissue. Sometimes they show inclusions of calcium salts. Such focal dissemination is called polymorphic.

The tendency to merge the foci and form the decay is poorly expressed, and therefore the decay cavities are formed slowly. They have certain characteristics.

Cavities are usually located in the upper lobes of both lungs, often symmetrically, their lumen completely free of caseo-necrotic masses; walls thin, perifocal infiltration and edema of surrounding tissues are absent. Such cavities are often called stamped, or spectacled, caverns.

Significant morphological changes in the lung tissue with a violation of its biomechanical properties lead to hypertension in a small circle of blood circulation, hypertrophy of the right ventricle and gradual development of the pulmonary heart.

As a result of repeated waves of hematogenous dissemination of Mycobacterium tuberculosis in patients with chronic disseminated tuberculosis of the lungs, extrapulmonary lesions are often formed: in the larynx, bones and joints, kidneys, genitals and other organs.

[17], [18], [19], [20]