Tuberculosis Study Guide - M. M. Savula 2002

Secondary forms of pulmonary tuberculosis
Tuberculous pleurisy

Tuberculous Pleurisy is a specific inflammation of the Pleura that may be accompanied by exudation into the pleural cavity.

It occurs in 2-6 % of tuberculosis patients. Among pleurisies of various etiologies, tuberculous pleurisy accounts for about 24 %.

Pathogenesis. Pleurisy is most commonly a complication of other pulmonary or extrapulmonary forms of tuberculosis, although it can also occur as an isolated form without visible involvement of other Organs. Mycobacteria can enter the pleura via lymphogenous, hematogenous, or direct contact routes. Triggering factors for The Development of pleurisy include hypothermia, hyperinflation, excessive physical exertion, and malnutrition. Normally, There is a small amount of serous fluid (1-2 ml) in the pleural cavity. During hypersensitization in response to infection, hyperemia and vasodilation of the visceral pleura occur. Fluid then transudes from these vessels into the pleural space. Concurrently, the absorptive capacity of the parietal pleura decreases, and after The formation of massive fibrin deposits on its surface, fluid absorption may cease entirely.

Based on pathogenesis, the following types are distinguished:

allergic pleurisy, as a manifestation of pleural hypersensitization to mycobacterial breakdown products, in which no mycobacteria are found in the pleural fluid;

perifocal pleurisy and pleural tuberculosis, in which tuberculous tubercles and other signs of specific inflammation are found on the pleural layers, leading to exudate formation.

If a cavity ruptures into the pleural space, its contents and air enter the cavity, resulting in purulent pneumopleurisy. If fistulas cannot be closed over a long period, chronic tuberculous empyema develops.

Clinical Features. Fibrinous (dry) and exudative pleurisies are distinguished. In Fibrinous pleurisy, moderate inflammatory changes and fibrin deposits occur in localized areas of the pleura. The MAIN CLINICAL MANIFESTATIONS of fibrinous pleurisy are pleural pain and a dry cough. The pain is localized to the site of the lesion. In apical pleurisy, it radiates along the Brachial Plexus. In interlobar pleurisy, the pain is located between the shoulder blades. In diaphragmatic and lower costal pleurisy, the pain may resemble that of biliary tract or Kidney diseases, while in left-sided costal pleurisy, it mimics angina pectoris. Bending the torso toward the healthy side intensifies the pain because friction between the pleural layers increases. Dry pleurisy begins gradually, accompanied by a slight decline in the patient's general condition and a low-grade fever. Physical examination reveals a slight lag of the affected side of the chest during breathing, limited mobility of the lower lung border on Percussion, and a pleural friction rub on Auscultation.

Exudative pleurisy is accompanied by the effusion of fluid (exudate) into the pleural cavity, which can be serous, sometimes serosanguinous, purulent, or rarely chylous (containing Lymph). The exudate can be free-flowing or loculated.

The onset of this form of pleurisy varies. Most often, the patient's well-being deteriorates over several days or sometimes weeks, presenting with recurrent side pain, occasional low-grade fever, and a cough. Subsequently, the Temperature rises sharply and the pain subsides, but dyspnea develops due to fluid accumulation in the pleural cavity. Less commonly, the disease begins acutely with a high fever, sharp chest pain, cough, and a significant decline in general condition. After a few days, the pain decreases while dyspnea worsens. A subclinical onset is also possible, where pleurisy runs its course with normal or low-grade temperature and minor general weakness.

Regardless of the onset, dyspnea worsens as the exudate accumulates. Patients typically lie on the affected side. With a significant amount of exudate, physical examination reveals a slight enlargement of the affected side of the chest, its lag during Respiration, and flattening of the intercostal spaces. Percussion over the exudate area yields a dull sound, and tactile fremitus and breath sounds are markedly diminished in the same region. Bronchial breathing can sometimes be heard above the fluid level. Large effusions may cause a shift of the cardiac borders to the opposite side and pronounced tachycardia. A pleural friction rub may be heard at the onset of exudate formation.

Analysis of the pleural exudate is essential for diagnosing pleurisy. In tuberculosis, the exudate is usually clear, sometimes opalescent, with a specific gravity of 1018-1025 and a protein content of 30-60 g/L. The Cell count exceeds 1-10⁹ /L. Initially, neutrophils may predominate (50-60 %), but as inflammation subsides, lymphocytes become dominant (90-95 %). If the exudate becomes purulent, the cell count, particularly of neutrophils, increases sharply.

If an effusion is present in the pleural cavity, its Etiology must be established. First, it is necessary to determine whether the fluid in the pleural cavity is an exudate or a transudate. An exudate results from an inflammatory process that increases the permeability of Blood Vessels and pleural layers, causing inflammatory fluid rich in protein and cellular elements to transude into the pleural cavity. The most common causes of exudate are tuberculosis, non-specific pleurisy, and Cancer. A transudate occurs in congestive Heart Failure, Liver cirrhosis, Nephrotic Syndrome, and Myxedema. It forms As a result of hemodynamic disturbances in circulatory failure, and Changes in the oncotic and hydrostatic pressure of Blood Plasma.

Class="center">Characteristics of transudate and exudate

Detection of MBT in the pleural effusion helps establish the Diagnosis, but a negative result does not rule out a tuberculous Water/144.html">Origin of the pleurisy.

In tuberculous pleurisy, peripheral blood tests may show moderate leukocytosis, an increased percentage of band neutrophils, and lymphopenia. ESR is elevated to 20-25 mm/h.

The reaction to the Mantoux test is usually positive or hyperergic, although the process can sometimes occur with negative reactions to tuberculin.

X-ray Examination in fibrinous pleurisy reveals restricted diaphragmatic movement. In exudative pleurisy, an intense homogeneous shadow is visible, predominantly in the posteroinferior and lateral Regions of the lung field. Its intensity decreases toward the Mediastinum and upward. The upper border of the opacity appears as an oblique curve with its highest point in the lateral regions, gradually sloping down toward the mediastinum (Damoiseau's line) (Fig. 21). With a significant amount of exudate, the mediastinal organs are shifted to the opposite side. An X-ray is believed to detect fluid in the pleural cavity if its volume is at least 200 ml.

Fig. 21. Chest X-ray. Right-sided exudative pleurisy.

The tuberculous nature of pleurisy is confirmed by:

1) the presence of tuberculous changes in the Lungs or other organs;

2) a pronounced reaction to the Mantoux test with 2 TU or a recent "conversion" of tuberculin Skin tests;

3) the predominantly serous Nature of the exudate with a predominance of lymphocytes, and the detection of MBT in the exudate (rarely);

4) in complex cases, a pleural biopsy is performed.

Sometimes, allergic tuberculous pleurisy responds rapidly to desensitizing therapy and broad-spectrum Antibiotics. Healthcare providers and the patient let their guard down and diagnose non-specific pleurisy. However, Pulmonary Tuberculosis often develops in such patients 2 to 3 years later. Therefore, if the etiology of pleurisy cannot be definitively established, it should be treated as tuberculous, and anti-tuberculosis therapy must be initiated.

Pleurisy is treated with anti-tuberculosis drugs for 5-6 months. Vitamins, desensitizing agents, and, in cases of large effusions, corticosteroids are prescribed. Pleural punctures to evacuate the exudate are required.

Pleural puncture

Pleural puncture is performed by a physician adhering to aseptic techniques. The puncture site is determined via fluoroscopy or percussion. In cases of significant free effusion, the puncture is performed after local anesthesia in the VII- VIII intercostal space along the scapular or posterior axillary line, over the upper edge of the underlying rib to avoid damaging the neurovascular bundle. The puncture needle must be connected to a rubber or plastic tube, closed with a clamp, with a cannula on the free end. At the moment the puncture needle enters the pleural cavity, the physician feels a "give" (loss of resistance). After this, a 20 ml syringe is attached to the tube, the clamp is removed, and the fluid is aspirated. Each time the syringe is filled, the tube is clamped, the syringe is disconnected, and its contents are emptied into a tray and a specially prepared sterile container. If necessary, the physician administers antibiotics into the pleural cavity.

The container with the pleural fluid and the corresponding referral form is sent to the laboratory. It is necessary to deliver all collected pleural fluid to the laboratory for the required analyses.

The following is The sequence of assistance provided by a junior medical professional during a pleural puncture performed by a physician.

Assisting the Physician During Pleural Puncture

Questions

1. What are the clinical manifestations of fibrinous and exudative pleurisy?

2. Which diseases are most commonly complicated by exudative pleurisy?

3. What suggests a tuberculous etiology of exudative pleurisy?

4. What materials need to be prepared for a pleural puncture?