Open access peer-reviewed chapter
Abstract
Pleural tuberculosis (TB) is the second most common extra-pulmonary form of TB, following tuberculous lymphadenitis. Pleural TB is most likely to occur due to the rupture of a subpleural caseous focus within the lung or, sometimes, due to the spread of infection from a lymph node into the pleural space. In pleural TB, it has been found that the delayed type of hypersensitivity (DTH) is responsible for the development of pleural effusion. Clinical manifestations mainly include pleuritic chest pain, nonproductive cough, anorexia, weight loss, night sweats, and in severe cases, dyspnea. Manifestations of pleural TB among HIV individuals depend on the CD4 count. A chest radiograph is the initial mode of investigation and is confirmed by USG thorax. Pleural fluid analysis helps in diagnosing and ruling out other causes of pleural TB. Levels of ADA and interferon gamma are helpful in establishing the diagnosis of pleural TB. Pleural biopsy culture, in combination with histopathological and molecular methods, can diagnose up to 95% of pleural TB. Anti-tuberculous drugs are the mainstay of therapy and the duration of treatment is 6 months. The role of corticosteroids is limited to certain situations only. Residual pleural fibrosis is the most common complication, while TB empyema is a severe form of complication.
Keywords
- pleural tuberculosis
- pleural effusion
- pleural TB
- tuberculosis
- Mycobacterium tuberculosis
1. Introduction
Pleural tuberculosis (TB) is the second most common extra-pulmonary form of TB, following tuberculous lymphadenitis. The incidence of pleural TB varies from 3 to 5% of tuberculous patients in non-endemic areas and can reach up to 30% in endemic areas [1, 2]. In countries like India, where there is a high burden of TB cases, the incidence of pleural TB varies from 30 to 80% of all pleural effusions and complicates 31% of Pleural TB [3]. The frequency of pleural TB depends on the prevalence of TB and HIV in a specific population. One should consider the diagnosis of TB in the presence of exudative pleural effusion.
2. Pathogenesis
Pleural TB is caused by
Pleural TB is most likely to occur due to the rupture of a subpleural caseous focus within the lung [4, 5], or sometimes due to the spread of infection from lymph nodes into the pleural space. This mechanism is more commonly observed in post-primary or secondary tuberculosis. Other postulated mechanisms include (1) hematogenous spread, as seen in the case of primary tuberculosis; (2) direct involvement of the pleura, which can occur in immunocompromised patients such as those with HIV/AIDS; and (3) spread from surrounding organ TB foci, such as TB spine, TB chest wall, or TB osteitis of the rib; (4) The involvement of peripheral interstitial lymphatics in TB may be responsible for the development of pleural effusion [6].
The development of pleural effusion depends on the rate of fluid formation and absorption. The formation of fluid depends on hydrostatic and oncotic pressure within the parietal and visceral pleura, as well as intrapleural pressure. Movement is governed by Starling’s law. Change in this equation results in the accumulation of fluid from either parietal or visceral pleural capillaries. Interstitial fluid typically originates from high pressure or high permeability pulmonary edema. Other less common sources of pleural fluid include intrathoracic lymphatic or blood vessels and the peritoneal cavity. Fluid is reabsorbed by pleural lymphatics primarily in the parietal pleura and capillaries of the visceral pleura.
In pleural TB, it has been found that the delayed type of hypersensitivity (DTH) is responsible for the development of pleural effusion. Direct infection in the pleural space is rarely observed. The patient developed a reaction to Mtb protein, which reached the pleural space through the mechanism mentioned above, resulting in an inflammatory reaction due to interaction with T-lymphocytes. An increase in vascular permeability leads to the extravasation of protein-rich fluid. Additionally, a high concentration of protein within the pleural space stimulates the accumulation of fluid [7]. It also found that the lymphatic system stomas present in the parietal pleura are obstructed due to inflammation, ultimately resulting in a reduced rate of pleural fluid clearance [8].
The immunological reaction in response to Mtb protein within the pleural space is no different from that seen in the case of pulmonary TB. Initially, neutrophils play an important role, followed by macrophages and lymphocytes. Ultimately, a granuloma is formed, which can be visible on the parietal and visceral pleura during thoracoscopy.
3. Clinical manifestations
Pleural tuberculosis is typically an acute illness and is commonly observed in younger populations as part of primary tuberculosis. In the older population, it occurs as a part of post-primary tuberculosis. Diabetes mellitus (DM), chronic alcoholism, immunocompromised conditions such as HIV/AIDS, malignancy, post-organ transplant, immunosuppressive therapy, chronic kidney disease, etc., are risk factors for pleural TB.
The presentation of pleural tuberculosis varies in duration, ranging from a few days to several weeks or even months. Patients usually experience a dry cough and pleuritic chest pain, which worsens with coughing or sudden movement and is sometimes relieved by lying on the same side. When a presentation is acute, the predominant symptom is chest pain. In a chronic course, symptoms are milder in nature. Fever is present and is usually low-grade. Other symptoms are nonspecific, such as anorexia, night sweats, fatigue, and weight loss [1, 4, 8]. Sometimes, patients may remain completely asymptomatic [1].
Physical examination findings in such patients are usually nonspecific. Mediastinal shift of the trachea to the opposite side, fullness of the intercostal space, and reduced tactile vocal fremitus may be observed. In percussion, a subtympanic note is present at the level of pleural effusion and a stony dullness note is present in the case of large or massive pleural effusion. The obliteration of Traube’s sign refers to the loss of the tympanic note in the left lower lung in the mid-axillary line, which is replaced by a dull note due to pleural effusion. The Ellis S-shaped curve sign is characterized by the highest dull note being present in the mid-axillary line and the lowest at the spine, assuming the shape of an S. This sign is observed in cases of moderate-sized effusion. Grocco’s triangle sign is observed in cases of moderate to large effusion, where an area of dullness or decreased resonance is detected contralateral to the effusion at the lower side. It occurs due to the shift of the posterior mediastinum. During auscultation, air entry may be reduced or absent on the side with effusion. One can hear pleural friction rub during an acute presentation. The Aegophony sign is present, and vocal resonance is reduced in pleural effusion. All of the above examination findings are nonspecific and may be present in other causes of pleural effusion.
3.1 In HIV-positive individuals
In certain geographic areas, the incidence of TB and pleural TB has increased, which is attributed to the rise in HIV infections. Initially, it was thought that pleural TB tends to occur in the initial phase of HIV infection. However, it was found that it is more common among patients with a CD4 count greater than 200 cells per mL-1 [9]. Manifestations of pleural TB among HIV individuals depend on the CD4 count. In such individuals, in addition to delayed-type hypersensitivity (DTH), the persistence of Mtb within the pleural space due to immune system failure is proposed as a factor in the development of pleural TB [10]. Clinical features in HIV-positive individuals are similar to those in HIV-negative individuals, but patients may present with atypical, longer duration of symptoms and more severe complications.
4. Investigations
Once a patient is suspected to have pleural TB based on clinical presentation and physical examination, the next most appropriate step is to perform imaging to confirm the presence of pleural effusion.
4.1 Radiology
4.1.1 Chest x-ray
A chest radiograph is the most cost-effective and widely available method for further evaluating suspected pleural TB. Pleural effusion in tuberculosis is usually unilateral [11] and is present in 90% of cases, but bilateral involvement may also occur (see Figures 1 and 2).
Figure 1.
Right side unilateral pleural effusion.
Figure 2.
Bilateral pleural effusion.
The chest x-ray in Figure 1 shows unilateral pleural effusion, which is more commonly found on the right side. In Figure 2, the chest x-ray shows bilateral pleural effusion, which is present in about 10% of cases.
The amount of pleural effusion in tuberculosis varies from minimal to mild and can be large or even massive, leading to severe breathlessness in some patients. The amount of fluid in pleural TB commonly varies from mild to moderate [12].
In Figure 3, the chest x-ray suggests a massive pleural effusion with a shift of the mediastinum to the opposite side. In Figure 4, the chest x-ray shows a typical type of pleural TB. Sometimes, patients may present with loculated pleural effusion, as seen in Figure 5.
Figure 3.
Massive pleural effusion.
Figure 4.
Mild to moderate pleural effusion.
Figure 5.
Left Loculated pleural effusion.
4.1.2 Ultrasonography
Ultrasonography (USG) of the thorax is the most accurate method for confirming the presence and quantifying pleural fluid. It can more accurately detect effusion than a chest radiograph, without any exposure to radiation (Figure 6).
Figure 6.
USG thorax appearance of pleural effusion.
On ultrasonography (USG), the most common findings in pleural TB are homogeneously echogenic, septated, or complex. The presence of echogenic material and septations is a common finding in subacute cases. USG can differentiate between thin or thick septa, the presence of loculation, and thin or thick fluid based on echogenicity. It can also identify the thickening of the pleura and guide the aspiration of deep-seated effusion as well as pleural biopsy.
4.1.3 Computer tomography
A thoracic computer tomography (CT) may be necessary for further evaluation of pleural tuberculosis, especially in complicated cases. A recent study shows that the presence of subpleural nodules and septal thickening is common in patients with pulmonary tuberculosis and pleural effusion [6].
Figure 7 depicts an axial view of pleural effusion indicated by the black arrow, while Figure 8 shows a sagittal view of pleural effusion also marked by a black arrow.
Figure 7.
Axial view of pleural effusion.
Figure 8.
Sagittal view of pleural effusion.
CT thorax is also helpful in detecting loculated pleural effusion and can be used for CT-guided aspiration in deep-seated pleural effusion. Figure 9 shows a loculated pleural effusion indicated by the black arrow. Sometimes, consolidation with a cavity and pleural effusion may be detected on a CT scan of the thorax (See Figure 10).
Figure 9.
Loculated pleural effusion on lateral aspect of chest wall (black arrow).
Figure 10.
Consolidation with cavity with contralateral pleural effusion.
4.2 Pleural fluid
Once fluid is present in the pleural space, the next step is to perform diagnostic or therapeutic thoracentesis, depending on the patient’s clinical condition. The definitive diagnosis of pleural TB is made by demonstrating Mtb bacilli within the fluid. It is difficult to isolate Mtb bacilli from pleural fluid because, in the majority of cases, the fluid accumulates as a result of delayed-type hypersensitivity (DTH) to the Mtb bacilli protein. There is no test for diagnosing pleural TB with 100% sensitivity and specificity. Diagnosing TB in pleural effusion is challenging and requires consideration of clinical features, radiological findings, and laboratory investigations to confirm the diagnosis. Once fluid is aspirated, the following investigations are conducted on the pleural fluid.
4.2.1 Total count (TC)
The total cell count (TCC) within pleural fluid is usually between 500 and 1000 cells per cubic millimeter (cmm). In pleural tuberculosis, the white blood cell count may be within the normal range or elevated. The investigation is nonspecific and may indicate other causes of pleural effusion. A high white blood cell count may raise suspicion of bacterial empyema or secondary infection in pleural TB.
4.2.2 Differential count (DC)
In pleural tuberculosis, the pleural fluid analysis within the first few days may show a neutrophilic response, followed by a predominantly lymphocytic response. Neutrophils serve as the first line of defense and respond initially. In the majority of cases, lymphocyte counts are more than 50% of the total count. Other cells that can be present include red blood cells (RBC), eosinophils, and mesothelial cells. RBCs may be present due to a traumatic tap, coexisting malignancy, or, rarely, pleural TB associated with hemorrhagic effusion. In pleural tuberculosis, there is a low number of mesothelial cells, mainly due to a decrease in shedding. Eosinophils are typically absent or present in low numbers. If there are high eosinophil levels, other possible causes need to be ruled out.
4.2.3 Biochemical analysis
The pH of the fluid is nonspecific and has no diagnostic value. The protein level in pleural tuberculosis is elevated, with levels found to be greater than 5 g/dL. The level of lactate dehydrogenase (LDH) is elevated, and once again, it is nonspecific. The levels of fluid protein and LDH, along with their serum levels, help establish the diagnosis of exudative pleural effusion using Light’s criteria. The sugar level in TB pleural effusion is usually within the normal range. A low sugar level suggests a secondary bacterial infection or an alternative diagnosis other than pleural TB. Elevated sugar levels may indicate a potential diagnosis of diabetes mellitus. All the above biochemical analyses are not useful for confirming the diagnosis, but they support the diagnosis of pleural TB.
4.2.4 Adenosine deaminase (ADA) level
Elevated ADA levels are useful for diagnosing pleural TB, in addition to other fluid analyses. ADA is an enzyme involved in the catabolism of purines. Elevated levels of ADA in plasma are an indicator of stimulated cell-mediated immunity, especially T-lymphocytes. The range of ADA levels varies from 30 to 70 U/L for diagnosing pleural TB. In a study, it has been found that patients with pleural TB have ADA levels greater than 70 U/L in pleural fluid [13], while ADA levels lower than 40 U/L can rule out the diagnosis of pleural TB [13, 14, 15]. Elevated ADA levels may also be present in other conditions such as bacterial empyema, parapneumonic effusion, malignant pleural effusion, and rheumatoid pleuritis, which make it nonspecific. By using a lymphocyte-to-neutrophil ratio of 0.75 or higher in pleural fluid, the specificity of ADA can be increased [16, 17, 18]. Recently, several studies have explored the use of the LDH/ADA ratio in diagnosing pleural TB, and they have demonstrated promising results. In various studies, the sensitivity has been shown to range from 86 to 89.1% and the specificity from 84.8 to 88%, depending on the ratio value ranging from 12 to 15 [19, 20]. Other studies have also suggested that it helps differentiate between pleural TB and malignancy [21]. However, further research is needed.
There are two isomers of ADA found in the body. ADA1 is found in all cells of the body, but it is primarily present in lymphocytes, neutrophils, and monocytes [22]. The ADA1 isoenzyme is elevated in pleural effusion other than tuberculosis. The ADA2 is mainly found in monocytes and comprises 90% of the ADA raised in tuberculous pleural effusion [22]. Measurement of both isomers and the ratio of ADA1/ADA2 may help confirm the diagnosis of pleural TB.
4.2.5 Interferon gamma level
The level of Interferon Gamma in pleural fluid may be useful in diagnosing pleural TB. Interferon gamma is produced by activated macrophages and CD4+ lymphocytes in response to Mtb protein in the pleural space [23]. It is measured in pleural fluid using enzyme-linked immunosorbent assay or radioimmunoassay. A newer method, the InterGam Rapid Immuno Suspension Assay, has been developed by Antrum Biotech. This method offers increased sensitivity, specificity, and rapid turnaround time [24]. Interferon gamma levels may be elevated in empyema.
Both measuring ADA and interferon gamma levels in pleural fluid can confirm the diagnosis of pleural TB with high precision. Due to its easy availability and cost-effectiveness, ADA is the first choice for investigating pleural effusion.
4.2.6 Pleural fluid tuberculous antigen or antibody detection
In the evaluation of pleural TB, the potential use of pleural fluid TB antigen or antibody was considered, but it did not yield any promising results.
4.2.7 Other biomarker levels
Interleukin (IL) 27, lysozyme, interferon gamma-inducible 10 kDa protein, neopterin, tumor necrosis factor alpha, matrix metalloproteinase, leptin, IL-1B, IL-2, IL-12, and fibronectin levels are among the biomarkers being investigated for potential use in diagnosing pleural TB.
4.2.8 Microbiological test
As previously discussed, Mtb is difficult to isolate from pleural fluid because it results from DTH to Mtb proteins. Sometimes, direct infection of the pleura with Mtb may result in fluid accumulation, and in such cases, bacilli can be isolated.
4.2.8.1 Microscopic examination
Pleural fluid staining for acid-fast bacilli (AFB) rarely yields any results and it is positive in less than 10% of cases. A concentration of 10,000 bacilli per milliliter (mL) is required for detection under microscopy. However, pleural fluid is a paucibacillary specimen, making it difficult to diagnose based solely on microscopic examination.
4.2.8.2 Polymerase chain reaction (PCR)-based tests
4.2.8.2.1 Cartilage-based nucleic acid amplification test (CBNAAT)
CBNAAT (Xpert MTB/RIF) is a sensitive method for detecting Mtb from biological specimens. It is a PCR-based method that detects Mtb deoxyribonucleic acid from a specimen. It is a more sensitive method than microscopic evaluation because it can detect approximately 100 bacilli per milliliter. The low number of Mtb in pleural fluid makes CBNAAT less sensitive. The meta-analysis study reported a mean sensitivity of 62% and a specificity of 98% [25]. A more sensitive method, Xpert Ultra, has been developed, and it can detect up to 20 bacilli per milliliter. It is a rapid method and the turnaround time is approximately 4 hours. In addition to detecting Mtb, it also detects the presence of rifampicin drug resistance within the specimen. Recently, there is a global trend of increasing drug-resistant tuberculosis, and this test is particularly useful despite its low sensitivity. If CBNAAT does not detect Mtb, it does not rule out the diagnosis of pleural TB. In such cases, ADA or interferon gamma levels are useful in establishing the diagnosis of pleural TB.
4.2.8.2.2 Line probe assay (LPA)
LPA is a PCR-based method that can simultaneously detect resistance to rifampicin and isoniazid. Turnaround time with LPA is approximately 72 hours. Its utility in the diagnosis of pleural TB is still under investigation.
4.2.8.2.3 Culture
The culture of microorganisms is the gold standard for diagnosing infections. One drawback of PCR-based methods is their inability to differentiate between live and dead organisms. The culture method is useful not only for diagnosis but also for follow-up cases of Pleural TB.
Various culture methods are available for Mtb. The Lowenstein-Jensen medium is the most widely used and cost-effective culture method. Newer methods such as the BACTEC-Mycobacteria Growth Indicator Tube (MGIT) are more rapid than the solid culture method and have a higher yield [26, 27].
In individuals with HIV, there is a high possibility of pleural fluid testing positive for acid-fast bacilli (AFB) and the isolation of Mtb on culture [28, 29]. If the CD4 count is less than 100 cells per mL−1, there is an increased possibility of AFB-positive pleural fluid [28].
4.3 Pleural biopsy
If pleural fluid analysis is non-diagnostic or if there is a need to rule out other causes, pleural biopsy is helpful in such situations. PCR-based methods can be used in pleural biopsy specimens and have identical or superior sensitivity compared to histopathological examination. It is prudent to use a combination of microbiological, histopathological, and PCR-based methods for the evaluation of pleural TB [30].
4.3.1 Transcutaneous closed pleural biopsy
A closed biopsy is taken from the pleura, either after marking the site using ultrasound of the thorax or under the guidance of thoracic ultrasound. There are various methods to use for biopsy.
4.3.1.1 Abram’s or cope needle
Both biopsy needles can be used blindly or under USG thorax guidance. The specimen is mainly obtained from the parietal pleura and multiple passes at multiple sites yield better results. The procedure is performed under local anesthesia and requires skill to conduct a biopsy. The bore of the needle is wider and may result in complications such as local pain, secondary infection, hemothorax, and pneumothorax. The rate of complications may be lower when using USG or CT guidance.
4.3.1.2 Automatic Bart biopsy gun
This gun is easy to operate due to its simplicity. It can be used blindly or under guidance. Its complication rate is the same as that of the above-mentioned needle.
4.3.2 Thoracoscopy/pleuroscopy
Pleural biopsy is obtained via thoracoscopy or pleuroscopy under direct visualization. Tubercles can be identified scattered over the parietal/visceral pleura, as well as septa within the pleural space, and biopsies can be taken. Sometimes, a parietal pleural biopsy may show no signs of pleural TB. In such cases, a visceral pleural biopsy may yield a diagnosis [31].
The pleural biopsy specimen can be used for microbiological examination, histopathological analysis, and culture. Staining of a pleural biopsy for AFB may show the organism in less than 10% of cases when no granuloma is present in the biopsy [4, 32]. Histopathological examination reveals granulomas within the biopsy of pleural TB, but granulomas may also be present in other conditions such as rheumatoid pleuritis, sarcoidosis, fungal infections, and sometimes in malignancy. Tuberculous granuloma is characterized by necrotizing caseating granulomas as caseous necrosis is not characteristic of other granulomatous inflammation. When pleural biopsy is used in conjunction with culture and histopathological examination, it can increase the chances of diagnosing pleural TB up to 95% [33].
4.4 Other
4.4.1 Sputum examination
Cough in cases of pleural effusion is usually dry, so it has no diagnostic value. When pleural effusion is associated with parenchymal lesions and a productive cough, sputum examination may detect Mtb using staining or molecular techniques, as mentioned above.
4.4.2 Tuberculin skin test
It is also known as the Mantoux test (MT). It has no diagnostic value in endemic areas where the prevalence of latent TB is high. When all investigations are inconclusive, the result of MT may support the diagnosis of TB. This test only indicates infection with Mtb but not the presence of the disease.
4.4.3 Interferon gamma release assay (IGRA)
The IGRA test measures the level of interferon gamma in response to stimulation with tuberculous antigen in the patient’s serum. As with MT, it has no diagnostic value in endemic areas and cannot identify disease, only infection. Both tests are useful in areas where the prevalence of TB is low.
Due to the paucibacillary nature of pleural effusion and the lack of a sensitive test for pleural TB, a definitive diagnosis is not made in many cases.
5. Treatment
Once a diagnosis of pleural TB is made based on clinical, microscopic, or molecular methods, the next step is to start anti-tuberculous drugs.
5.1 Anti-tuberculous treatment
Anti-tuberculous drugs are the mainstay of treatment for pleural TB. If PCR-based methods are used for evaluation and yield inconclusive results or confirm drug-sensitive Mtb, a combination of isoniazid, rifampicin, ethambutol, and pyrazinamide is suggested. The combination of these four drugs is administered for 2 months, followed by 4 months of isoniazid, rifampicin, and ethambutol [34]. Pleural TB in HIV patients remains the same as in non-HIV patients. The response to the treatment is indicated by the resolution of fever, a decrease in the frequency and severity of cough, a reduction in the severity of chest pain, and an improvement in appetite. These changes are usually noticed within 2 weeks of treatment. The resolution of pleural fluid occurs within 6 to 12 weeks after starting treatment, depending on the amount of fluid, presence of septation, and associated comorbidities such as DM.
If a PCR-based method suggests drug-resistant tuberculosis, the choice of drugs is based on the pattern of drug resistance identified by the PCR-based method and the results of the drug sensitivity test (DST) culture. The combination of drugs and duration of treatment varies according to the geographic area and the prevalence of drug-resistant tuberculosis.
5.2 Anti-inflammatory drugs
Corticosteroid treatment is not recommended for pleural TB. In certain situations, when patients experience severe symptoms such as chest pain, fever, or breathlessness that interfere with their daily lives, corticosteroids are administered. If necessary, it should be administered along with anti-tuberculous drugs at a dose of 0.5–0.75 milligrams per kilogram, followed by rapid tapering [8].
Serratiopeptidase is a proteolytic enzyme that possesses anti-inflammatory, anti-fibrotic, and analgesic properties [35]. The role of the anti-inflammatory drug serratiopeptidase has been shown to improve clinical outcomes and avoid surgery in cases of hydropneumothorax caused by tuberculosis, when used in conjunction with anti-tubercular drugs [35]. However, its study in pleural effusion is lacking. In certain situations, when corticosteroid use is contraindicated, and there are high TC in pleural fluid and severe symptoms, this drug may be useful. However, further studies are required.
5.3 Surgery
Surgery plays a limited role in the management of pleural TB. Surgical management in the form of thoracentesis or insertion of an intercostal drainage tube (ICD) may be necessary. Thoracentesis may be required in patients with a large effusion and shortness of breath to relieve symptoms. When thoracentesis is used in conjunction with anti-tuberculous drugs and corticosteroids, faster resolution of symptoms occurs [36, 37].
ICD insertion is necessary in cases of massive pleural effusion requiring immediate relief, pus formation, or failure to resolve due to excessive septation within the pleural cavity. The use of intrapleural fibrinolytic drugs is beneficial in terms of rapid drainage and resolution on chest radiograph, improvement in symptoms, reduction in the time from treatment to drainage, and improvement in forced vital capacity and total lung capacity at the end of treatment [38, 39, 40, 41, 42]. Fibrinolytic drugs primarily break down septa and liquefy fluid, resulting in the rapid clearance of fluid.
Thoracoscopy is required when pleural TB is complicated by loculated pleural effusion, thickened calcified pleura, pus formation, and excessive septa that do not respond to fibrinolytic therapy.
5.4 Follow-up
Follow-up of patients with pleural TB is required to evaluate the resolution of symptoms, the resolution of pleural fluid, and any adverse effects of anti-tuberculous treatment. If resolution of symptoms or pleural fluid does not occur, then alternative or additional diagnoses need to be investigated.
6. Complications
Residual pleural thickening is the most common complication found in patients with pleural TB. More than 2 mm of residual remains visible on the chest radiograph and CT scan after 24 weeks of treatment [35]. Fibrothorax is a severe form of thickening that occurs when pleural TB remains inadequately treated, untreated, or in patients with TB empyema. Calcification of residual pleural thickening may be noticed on chest radiographs. Due to residual pleural thickening, the patient may experience intermittent or persistent chest pain on the side of the effusion. Restrictive pulmonary function abnormalities may occur in such patients. Decortication is necessary in severe cases to alleviate restrictive changes. TB empyema may develop as a complication of pleural TB or as a distinct entity.
7. Conclusion
Pleural TB is the second most common extra-pulmonary form of tuberculosis, following TB lymphadenitis. Pleural TB is most likely to occur due to the rupture of a subpleural caseous focus within the lung or sometimes due to the spread of infection from a lymph node into the pleural space. DTH is a mechanism by which fluid accumulates within the pleural space, but it is rarely due to direct infection with Mtb. It is a disease that affects the young population. The presentation may be acute to subacute and symptoms can range from pleuritic chest pain, nonproductive cough, anorexia, weight loss, night sweats, and dyspnea in severe cases. Evaluation methods include radiological imaging, pleural fluid analysis using molecular and culture methods, pleural biopsy, and sputum examination. Anti-tuberculosis drugs are the mainstay of treatment and the choice depends upon DST results. Thoracentesis and ICD insertion may be required in severe cases. Residual pleural biopsy is the most common form of complication.
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