Tuberculous pleurisy

Tuberculous pleurisy is an acute, subacute, chronic or relapsing tubercular inflammation of the pleura that can occur as a complication in any form of tuberculosis.

The most common pleurisy is observed with pulmonary tuberculosis. Occasionally it can also take place as an independent clinical form, i.e. Without clearly defined tuberculosis lesions of other organs, and be the first clinical manifestation of tuberculosis infection in the body.

Epidemiology of tuberculous pleurisy

In Ukraine and Russia, tuberculosis etiology is noted in almost half of all patients with exudative pleurisy. In newly diagnosed TB patients with respiratory organs, tuberculous pleurisy is diagnosed in 3-6% of cases, more often in children, adolescents, young people. In the structure of the causes of death from tuberculosis pleurisy is about 1-2%, and in the main it is chronic purulent pleurisy.

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

Pathogenesis and pathological anatomy of tuberculous pleurisy

Pleurisy complicates the course of tuberculosis of the intrathoracic lymph nodes, the primary complex, disseminated tuberculosis. In the pathogenesis of pleurisy, great importance is attached to the preliminary specific sensitization of the pleura, as an important condition for the development of inflammation under the influence of mycobacteria. An important role in the pathogenesis of tuberculous pleurisy is played by the close anatomical and functional interrelation of the lymphatic system of the lungs and the pleura.

Tuberculous pleurisy can be allergic (paraspecific), perifocal and flow in the form of pleural tuberculosis. Depending on the nature of pleural contents, tubercular pleurisy can be dry (fibrinous) and exudative. Purulent exudative pleurisy is called tubercular empyema of the pleura.

Allergic pleurisy occurs as a result of hyperergic exudative reaction of pleural sheets to tuberculosis infection. This reaction is observed mainly in primary tuberculosis, which is characterized by high sensitization of many tissues, including serous membranes. Pleural serous or serous-fibrinous exudate forms in the pleural cavity, fibrin overlays on the pleura appear. Cellular composition of exudate is lymphocytic or eosinophilic. Specific tuberculosis changes are not detected, or single tubercular tubercles are found on the pleura.

Perifocal pleurisy develops in cases of contact lesion of pleural sheets from subpleurally located sources of tuberculous inflammation in the lung. It is observed in patients with a primary complex, disseminated, focal, infiltrative, cavernous tuberculosis. First, the pleural lesion is local, with the deposition of fibrin, but then there is serous or serous-fibrinous exudate.

Tuberculosis of the pleura occurs in different ways: lymphogenous, hematogenous and contact. It can be the only manifestation of tuberculosis or it can be combined with other forms of the disease.

With lymphogenous or hematogenic infection, pleural flukes develop on pleural sheets, and serous-fibrinous exudate appears in the pleural cavity. In cases of progression of the process and the disintegration of tubercular granulomas, the effusion becomes hemorrhagic. With the involution of the process, the effusion resolves, the pleural sheets thicken, the pleural cavity partially or completely obliterated.

The contact path for the development of pleural tuberculosis is observed with subpleural localization of tubercular inflammation in the lung, which, as a rule, extends to the pleural sheets. In most patients, pleural damage is limited to a local inflammatory response. On the visceral pleura appear tubercular eruptions, fibrinous overlap, granulation tissue, in the pleural cavity there may be an effusion. In the organization of fibrin and granulation, fusion between the leaves of the visceral and parietal pleura is formed. Less often contact tuberculosis lesions of the pleura are accompanied by the formation of a large amount of serous or serous-fibrinous exudates with predominantly lymphocyte composition. Degradation of exudate is completed by the formation of fibrous depositions on the pleura, especially pronounced in pleural sinuses.

Another variant of the contact path for the development of pleural tuberculosis is the direct entry of infection into the pleural cavity from the affected lung. It occurs in cases of disintegration of subpleurally located caseous masses or perforation of the pulmonary cavity into the pleural cavity. Through the opening in the cavity of the pleura penetrate the caseous masses, the contents of the cavity and often air. The pleural cavity is infected with mycobacteria, the lung is partially or completely subside, and an acute tuberculosis empyema develops. A condition in which pleural cavity is simultaneously detected by pus and air is called pyopneumotorax.

With the continued communication of the cavity with the pleural cavity, chronic tuberculosis empyema with bronchopleural fistula is formed. The leaves of the parietal and visceral pleura in chronic tuberculosis empyema are sharply thickened, hyalinized, calcified. Their surface is covered with caseous-necrotic and fibrinous-purulent masses. A tuberculosis infection is usually associated with a nonspecific purulent flora. Patients with chronic tuberculosis empyema often have amyloidosis of internal organs.

The cure of tuberculous pleural empyema results in the formation of extensive pleural overlap (shvart), obliteration of the pleural cavity and fibrotic changes in the lung and chest wall.

Symptoms of tuberculous pleurisy

The clinical picture of tuberculous pleurisy is diverse and closely related to the peculiarities of tubercular inflammation in the pleural cavity and lungs. In some patients, other manifestations of tuberculosis, especially primary (paraspecific reactions, specific bronchial lesions) are noted simultaneously with pleurisy.

Allergic pleurisy begins acutely. Patients complain of chest pain, shortness of breath, fever. In blood tests, eosinophilia and an increase in ESR are typical. Exudate is serous, with a large number of lymphocytes, mycobacteria can not be detected. With videotorakoscopy, there may be a hyperemia of the pleural sheets. Anti-tuberculosis chemotherapy in combination with anti-inflammatory and desensitizing agents usually leads to an improvement in the condition and recovery without gross residual changes in the pleural cavity.

Perifocal pleurisy begins gradually or subacute with the appearance of pain in the chest, dry cough, unstable subfebrile body temperature, a slight weakness. Patients often refer to previous hypothermia and influenza as factors that trigger the development of the disease. Pain in the side becomes worse when coughing, tilting in the opposite direction. Characteristic signs are the limitation of the mobility of the chest when breathing on the side of the lesion and the noise of friction of the pleura. Noise persists for several days, and then disappears under the influence of treatment or even without it. Sensitivity to tuberculin in dry tuberculous pleurisy is high, especially in children. When percussion, if there is no significant lesion of the lung, no changes are detected. On the radiographs, local tuberculosis lesions of the lungs, pleural compaction and pleural fusion in the form of low intensity darkening areas are detected. Only on CT is more clearly defined inflammatory and fibrous consolidation of pleural sheets.

As the exudate accumulates in the pleural cavity, the pain gradually weakens, the pleural friction disappears and typical physical, echographic and radiographic signs of exudative pleurisy appear. Exudate is serous with a predominance of lymphocytes and a high content of lysozyme. Mycobacteria in exudate are absent. When videotorakoscopy, changes in the visceral pleura over the affected lung zone are noted: hyperemia, thickening, fibrin films. The course of perifocal pleurisy is usually prolonged, often recurrent.

Tuberculosis of the pleura with exudative pleurisy can manifest itself as a clinical picture of varying severity. Most patients have symptoms of intoxication within 2-3 weeks. Then the body temperature rises to febrile values, dyspnea appears and gradually builds up, there is a constant pressing pain in the side. In the early period of the inflammatory process, before separation of the pleural sheets with exudate, there is a noise of friction of the pleura. It can be accompanied by small bubbling wet and dry rales. As the fluid accumulates during exudative pleurisy and pleural empyema, the classical clinical picture develops, the ore wall on the pleurisy side lags behind when breathing. In cases of a large pleural effusion intercostal gaps are smoothed. The characteristic physical symptoms are a shortened or dull percussion sound, a weakening or absence of vocal jitter and respiratory noise over the area of the lesion. In the period of resorption of exudate, when pleural sheets begin to touch each other, again often listen to the noise of friction of the pleura.

The condition of patients is most severe with empyema of the pleura. Characterized by high body temperature, shortness of breath, night sweats, severe weakness, weight loss. If the exudate is not removed from the pleural cavity, it can fill the entire hemithorax and cause displacement and compression of the mediastinal organs with the development of pulmonary heart failure. This situation serves as an indication for the urgent removal of fluid from the pleural cavity.

Typical complications of tubercular empyema of the pleura include a breakthrough of purulent exudate in the bronchus or through the inter-ridge interval. With the breakthrough of pleural contents in the bronchus, the patient emits pus with a cough, sometimes in large quantities. There is always the danger of aspiration pneumonia. In the future, pleurobronchial fistula may form.

Diagnosis of tuberculous pleurisy

Changes in hemogram parameters in pleurisy correspond to the severity of inflammation of the pleura. Until the resorption of exudate in patients with tuberculous pleurisy constantly increase the ESR (from 50-60 mm / h in the acute period to 10-20 mm / h with resorption). In the early stage of serous or serous-fibrinous pleurisy, moderate leukocytosis is observed, an increase in the number of stab neutrophils, eosinopenia and lymphopenia, with hemorrhagic pleurisy and pleural empyema - pronounced leukocytosis.

In cases of rapid accumulation and repeated removal of exudate, hypoproteinemia develops in patients. Other types of exchange may be violated.

Very informative for exudative pleurisy X-ray and ultrasound. As the accumulation of exudate disappears, the transparency in the region of the rib-diaphragmatic sinus, and the shadow of the fluid is detected above the diaphragm. With an increase in the volume of liquid in the vertical position of the patient, a picture typical of free exudate is found for the dimming of the lower parts of the pulmonary field with a parabolic upper border running from above, from the outside downwards and inwards. Exudate shadow is intense and uniform. With a significant volume of fluid mediastinal organs are displaced in the opposite direction. Free pleural effusion can be detected with ultrasound and CT: the liquid is located in the back of the thoracic cavity and has a typical appearance of the half-oval. If there is air in the pleural cavity that can penetrate it through the bronchopleural fistula or accidentally during a pleural puncture, the upper boundary of the liquid remains in a horizontal position, regardless of the position of the patient's body (pneumoplethritis, pyopneumothorax). During fluoroscopy, when the patient moves, fluid fluctuations can be seen. The degree of decrease in lung and fusion between the visceral and parietal pleura is clearly defined by CT.

With the delimitation of one or more fluid accumulations by pleural fusion, a pleural effusion is formed (apical, paracostal, paramediastinal, supidiaphragmatic, interlobar). In such cases, the shape of the shadow does not change when the position of the body changes. Patients with tampered pleurisy, as a rule, have already been treated for tuberculosis, and in the lungs and pleural cavity they have residual post-tubercular changes.

To confirm the presence of a peribronchial fistula, a test with a paint is very informative: after injection into the pleural cavity during a puncture 3-5 ml of a methylene blue solution, sputum is stained. If the fistula is of considerable diameter, auscultation can listen to amphoric breathing, and when bronchoscopy, you can see the flow into one of the bronchi of pleural contents (with pneumocleitis - with air bubbles). X-ray examination in the vertical position of the patient allows to detect a decrease in the lung and horizontal level of fluid in the cavity of the pleura. The fistula opening from the pleural cavity can be detected by videotorakoscopy.

When pus breaks through the inter-ridge interval, it can collect under the surface layer of the muscles of the chest wall or in the subcutaneous tissue (Empyema necessitasis) or break through the skin outward with the formation of the pleurotora (pleurotical) fistula. Occasionally two fistulas arise successively: pleurobrochial and pleurotoral.

[9], [10], [11], [12]

Treatment of tuberculous pleurisy

• Tuberculosis - Treatment
• Chemotherapy for tuberculosis
• Anti-TB drugs
• Surgical methods of treatment of tuberculosis
• Pathogenetic therapy of tuberculosis
• Immunotherapy in the treatment of tuberculosis
• Physical methods of treatment of tuberculosis
• Methods of extracorporal hemocorrection in tuberculosis