Tuberculosis - I.T. Piatnochka 2005

Primary tuberculosis
Disseminated pulmonary tuberculosis

Disseminated Pulmonary Tuberculosis is a clinical form of tuberculosis resulting from lymphohematogenous spread of the infection and characterized by bilateral, symmetrical focal lesions predominantly localized in the upper, subcortical Regions of the Lungs.

Currently, among newly diagnosed pulmonary tuberculosis patients, the disseminated form accounts for 23%.

Pathogenesis. The Development of disseminated pulmonary tuberculosis requires the following conditions: the presence of a tuberculous lesion focus in the body, bacteremia, body hypersensitivity, and, above all, increased permeability of the pulmonary vessel walls, as well as reduced body resistance due to various provoking factors. The specific lesion focus is primarily a tuberculous lesion of the intrathoracic Lymph Nodes, from which MTB enter the right side of The Heart via the Thoracic duct and subclavian vein, and subsequently into the pulmonary artery and lungs.

In addition to lymphohematogenous dissemination, disseminated tuberculosis can result from the spread of MTB via bronchogenous or mixed pathways, which explains the symmetrical or asymmetrical nature of lung involvement. Depending on the massiveness and virulence of the infection, the condition of the macroorganism, and various negative provoking factors, acute, subacute, or Chronic disseminated pulmonary tuberculosis may develop. Depending on The pathway of MTB dissemination, these forms can be of hematogenic or lymphobronchogenic origin.

Acute disseminated tuberculosis of hematogenic origin most frequently manifests as Miliary tuberculosis (see “Miliary Tuberculosis”). It is distinguished as a separate clinical form due to its increased frequency under modern conditions and the worsening epidemiological situation regarding tuberculosis.

Subacute disseminated tuberculosis develops against the Background of reduced bodily resistance, has a severe progressive course—sometimes resembling Caseous Pneumonia—with a fatal outcome in 6 months or more (Fig. 14).

Pathomorphology. The main constituent elements of subacute disseminated tuberculosis are specific granuloma (tubercle), vasculitis, and alveolitis, which serve as the basis for The formation of large exudative foci in the upper and middle lung fields or throughout all pulmonary fields. Against the background of these foci, thin-walled cavities with perifocal inflammation may form. These cavities are more frequently located in symmetrical areas of the lungs. Extrapulmonary lesions are possible.

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Fig. 14. Disseminated pulmonary tuberculosis (subacute). Plain chest radiograph

Clinical Features. Main syndromes include intoxication and bronchopulmonary syndromes, as well as signs of other organ involvement.

Laboratory tests typically reveal pronounced pathological Changes in the hemogram. MTB are frequently detected in the sputum. The Mantoux test with 2 TU is positive, although it may be negative if the patient's condition is severe.

Radiologically, the foci are large, symmetrically distributed, of medium to low intensity, with blurred margins, prone to coalescence (resembling a “falling snow” pattern) and the formation of disintegration cavities, which eventually form “punched-out” cavities.

Differential Diagnosis is performed with pulmonary diseases that share similar radiological features accompanied by a dissemination syndrome and pulmonary congestion (there are over 200 such conditions). These primarily include bilateral Focal Pneumonia, sarcoidosis (stage II), carcinomatosis, silicosis, pulmonary congestion, idiopathic fibrosing alveolitis, Goodpasture syndrome, mucoviscidosis, pulmonary Toxoplasmosis, histiocytosis X, Pulmonary Thromboembolism, pulmonary candidiasis, periarteritis nodosa, Wegener's granulomatosis, alveolar proteinosis, etc.

Treatment. The primary method of treating patients with Subacute disseminated pulmonary tuberculosis is antimycobacterial therapy lasting 8–12 months. For the first 2–3 months, 4 antituberculosis drugs are used, followed by 3 drugs until the disintegration cavities close. Subsequent treatment is carried out with isoniazid and rifampicin or ethambutol (see “Treatment of tuberculosis”).