Tuberculous pleurisy is a common form of extra-pulmonary tuberculosis, which is an inflammation of the pleura caused by the entry of Mycobacterium tuberculosis and its metabolites into the pleural cavity in a hypersensitive state. The development of tuberculous pleurisy is closely related to Mycobacterium tuberculosis infection and the immune status of the body. Tuberculous pleurisy belongs to type V of the five major types of pulmonary tuberculosis, which is not a pulmonary lesion but is closely related to pulmonary tuberculosis in clinical practice. Tuberculous pleurisy can occur after primary infection with Mycobacterium tuberculosis or at any stage of the course of tuberculosis disease. It can be divided into tuberculous dry pleurisy, tuberculous exudative pleurisy, and tuberculous pustulosis according to the clinical course and pathological manifestations. Because dry tuberculous pleurisy and exudative pleurisy are two stages of one disease, the former has a short course, while the clinical course and pathology of exudative pleurisy are more distinct, so the clinical course of the former is often obscured by the latter, so clinically dry tuberculous pleurisy and exudative pleurisy (abbreviated as dry pleurisy and exudative pleurisy) are often referred to as tuberculous pleurisy. I. Pathogenesis and pathophysiology I. Pathogenesis and pathophysiology Anatomy suggests that a hypothetical pleural cavity with negative pressure atresia is formed between the dirty pleura and the wall pleura on the left and right sides of the body, and the left and right pleural cavities are not connected to each other. Under normal conditions, the two pleural layers are in close proximity to each other and are lubricated by physiological fluid (about 0.3 ml/kg body weight). When Mycobacterium tuberculosis and its metabolites enter the pleural cavity in a highly sensitive state, it rapidly causes an inflammatory reaction in the pleura. It often occurs after the primary infection of Mycobacterium tuberculosis or occurs during the deterioration and relapse stage of tuberculosis. Second, the pathway of Mycobacterium tuberculosis reaching the pleura 1. When lymphatic dissemination pulmonary hilar or mediastinal lymph node tuberculosis, lymph node enlargement and compression affect the lymphatic fluid reflux, and due to the obstruction of drainage leading to lymphatic fluid reflux, Mycobacterium tuberculosis reaches the pleura directly and pleurisy occurs. Tuberculous granuloma of the wall layer pleura is also an important cause of tuberculous pleurisy due to obstruction of drainage of pleural effusion. The infiltration and destruction of tuberculosis lesions in any part of the body allows Mycobacterium tuberculosis to enter the blood circulation, resulting in the systemic hematogenous dissemination of Mycobacterium tuberculosis, which can cause tuberculous pleurisy when it invades the pleura. 3.Direct spread of Mycobacterium tuberculosis in the foci of intrapulmonary tuberculosis, rib, sternum and spine, paravertebral cold service swelling, chest wall tuberculosis and other foci near the pleura directly spread to the pleura. When the pleura is infected with Mycobacterium tuberculosis, congestion, edema, and fibrin exudation occur, resulting in dry tuberculous pleurisy. As the disease progresses, there are two types of regression, one is the dissipation of the lesion or the thickening and adhesion of the pleura. Second, because the body is highly allergic to Mycobacterium tuberculosis and its metabolites, the progression of the disease leads to a large number of exudative changes in the pleura, at this time, in addition to fibrinous exudation on the pleural surface, and the formation of plasmacytotic exudate and tuberculosis nodules, the exudate gradually increases, and the development of exudative pleurisy. Once exudative inflammation occurs in the pleura, pleural fluid will be continuously generated and absorbed. The formation and absorption of pleural fluid depends on the amount of pleural exudate and the speed of pleural fluid discharge through the lymphatic vessels of the pleural wall and the degree of lymphatic vessel patency. At present, there are new advances in the study of the mechanism of pleural effusion formation, and the theory of Starling’s law that “the wall pleura produces pleural effusion and the dirty pleura absorbs pleural effusion” has been revised, and recent studies have shown that pleural effusion is mainly produced by the wall pleura in the apical region of the thoracic cavity. Under normal conditions, due to the existence of a vertical gradient in the pleural cavity pressure, pleural effusion is generated from the parietal region of the thoracic cavity and flows in the direction of the bottom of the thoracic cavity, and eventually the pleural effusion needs to be discharged through the bottom of the thoracic cavity, mainly by reabsorption from the lymphatic pores on the diaphragmatic and mediastinal surfaces of the wall layer pleura. The lymphatic pores of the wall pleura are connected to the lymphatic space, so the pleural fluid and the protein and cells in the pleural fluid are reabsorbed by the lymphatic pores of the wall pleura and discharged through the lymphatic vessels. The dirty pleura lacks lymphatic pore structure and is not connected to the lymphatic space, so the dirty pleura has almost no effect on the formation and absorption of pleural effusion. Under normal conditions, the lymphatic clearance of the mural pleura increases with the increase of pleural effusion, aiming to keep the volume of the pleural cavity constant. Recently, Negrini et al. demonstrated that the pressure in the subpleural lymphatic vessels of the mural layer is lower than the pleural effusion pressure, and due to the pressure difference, the pleural effusion flows from the pleural cavity to the mural pleural lymphatic network. When inflammation occurs in the pleura, on the one hand, the secretion of pleural fluid increases a lot and exceeds the maximum pleural lymph flow, and at the same time, tuberculous granuloma compresses the pleural lymphatic network or lymphatic vessels are pathologically blocked, resulting in a decrease in the discharge volume and causing the accumulation of pleural fluid. Clinical manifestations: 1. Dry pleurisy Mild dry pleurisy has a low metabolic response to Mycobacterium tuberculosis and may have no obvious clinical symptoms, or only a slight fever and mild chest pain which is often neglected, and some patients may show high fever and obvious severe chest pain. The chest pain is often sharp and pinprick-like, aggravated by deep inspiration and coughing, and the extent of pain depends on the site of inflammation involvement. In the case of costal pleurisy, the wall pleural nerves are involved, and the intercostal nerves and spinal nerves can be affected, causing pain in the chest and back; in the case of diaphragmatic pleurisy, the phrenic nerves are stimulated and further spread to the phrenic nerves, causing neck and shoulder pain, and sometimes upper abdominal pain; in the case of mediastinal pleurisy, pain in the anterior chest and sternum is caused; in the case of interlobular pleurisy, there is often no significant chest pain. Physical examination; shallow breathing, localized pressure pain and hypopnea on the affected side, pleural friction sounds can be heard, and inspiration and expiration are more pronounced. The clinical course of dry pleurisy is brief, usually turning into exudative pleurisy in 1 to 2 days. 2, exudative pleurisy Most exudative pleurisy is a continuation of dry pleurisy, and the early course of dry pleurisy in patients with exudative pleurisy is often overlooked or undetected. Exudative pleurisy manifests as a rapid onset, high fever, with body temperature mostly ranging from 38°C to 40°C, which can last for several days or even weeks, and the temperature is often proportional to the amount of fluid accumulation. Patients may have general malaise, malaise, night sweats, loss of appetite, and other symptoms of tuberculosis toxicity. In the early stage, chest pain and dry cough may appear when the effusion is small. With the gradual increase of pleural effusion, the wall pleura and the dirty pleura are separated by it, and the chest pain disappears and the dyspnea becomes more and more obvious, the degree of which is related to the amount of effusion. The more rapid the formation of effusion, the more obvious it is. Physical examination; early respiratory kinetics are reduced, pleural friction sounds can be heard, and friction sensation can be palpated; in the case of massive effusion, the affected side of the thorax and intercostal space is full, and respiratory motion is reduced; apical pulsation and trachea are displaced to the healthy side, and the effusion area is percussed with turbid or solid sounds, and the hepatic turbid zone can disappear if it is on the right side, and the Traube’s tympanic zone decreases if it is on the left side; fibrillation and breath sounds are reduced or disappeared. Interlobular effusion and basilar effusion signs are not obvious. V. Ancillary tests: Laboratory tests ( a ) Routine blood tests: normal or high total white blood cell count, increased sedimentation. ( B ) Pleural effusion examination of tuberculous pleurisy is exudate. ( C ) Pleural effusion routine examination 1. Appearance is mostly straw yellow, transparent or slightly mixed, easily coagulated. A few of them are yellow and light red, about 10% of pleural effusion is bloody, and the incidence of bloody pleural effusion in elderly patients with tuberculous pleurisy can reach 23.6%. Specific gravity 1. 018, pH 7. 0-7. 3, if pH is low, it indicates the tendency to develop into encapsulated effusion and pus. 3.Total cell count (100-500)X106/L, mainly neutrophils in the acute phase, gradually changing to monocytes, and mainly lymphocytes in the chronic phase. Mesothelial cells <5% (large amount of fibrin exuded from the pleural surface, preventing mesothelial cells from entering the pleural cavity). 4.Total protein Total protein >30g/L, Pleural fluid protein/serum protein >0.5. Glucose is mostly below 2.5 mmol/L. It is now recognized that glucose is not a sensitive indicator for the diagnosis of tuberculous pleurisy. ( D ) Mycobacterium tuberculosis examination Pleural fluid smear antacid staining for Mycobacterium tuberculosis, the positive rate is low about 5%, pleural fluid culture positive rate is only 25%, so the diagnosis of tuberculous pleurisy can not be based solely on pleural fluid smear and culture for Mycobacterium tuberculosis. (E) Pure protein derivative (PPD) skin test A positive PPD skin test indicates susceptibility to Mycobacterium tuberculosis, and the stronger the reaction, the greater the possibility of infection by Mycobacterium tuberculosis. Usually >15 mm in diameter or blisters are considered to be newly infected. It can help diagnose the presence or absence of TB infection. ( VI ) Pleural fluid polymerase chain reaction (TB-PCR) has a sensitivity of 52% to 81% and a high specificity (100%), with results available in 2 to 3 days, with false negatives and false positives reported, and is one of the important diagnostic methods when the positive rate of pleural fluid Mycobacterium tuberculosis examination is very low. ( VII ) Pleural effusion adenosine deaminase (ADA) ADA is an important enzyme of T lymphocytes. The activity is increased in all cellular immune diseases, and more markedly in tuberculosis. In tuberculous pleurisy, pleural fluid ADA is elevated. The diagnostic threshold is ADA > 45 U/L. Pleural effusion (P) ADA/serum (S) ADA>1 is more valuable, and is important in the diagnosis of tuberculous pleurisy. In the case of cancerous pleural effusion, ADA is lower, which can distinguish tuberculous pleural effusion from cancerous pleural effusion. X-ray examination ( a ) dry pleurisy Generally no X-ray changes. When the pleural fibrin deposition is 2-3mm, the chest film can be seen to have reduced translucency. In the case of basilar pleurisy, decreased movement of the affected diaphragm is seen on chest radiograph. (b) Exudative pleurisy varies according to the volume of fluid accumulation, with a small volume of fluid (300 ml) accumulating in the posterior costo-diaphragmatic sinus, only the costo-diaphragmatic angle is blunted on posteroanterior X-ray, and the posterior diaphragmatic angle is filled on lateral X-ray. In moderate amounts of fluid accumulation, a uniform density shadow is seen, with an arc of increased density along the chest wall from the top down to the diaphragmatic surface, with the concave surface facing the hilum. In large amounts of fluid, the entire affected side is dense, and the mediastinum is shifted to the healthy side, sometimes only the lung tip is translucent. CT scan of the chest has a high resolution and can detect a fluid volume of 15-20 ml, while a pleural fluid volume of at least 250 ml can only be detected on a chest X-ray. Some special types of pleurisy, such as interlobular pleurisy, encapsulated pleurisy, and mediastinal pleurisy, are more clearly shown on CT films, which can also detect pulmonary lesions obscured by effusion and are clearly localized, facilitating differentiation from other diseases. CT-guided aspiration and pleural biopsy are more accurate than other methods. The CT film of a small amount of effusion shows a crescent-shaped curved high-density shadow in the lower posterior part of the chest cavity, with uniform density, clear and smooth edges, and a concave surface forward, and the CT value is slightly higher than that of water. A large amount of effusion can be seen as a solid density shadow with compression of lung tissue under the dirty layer of pleura, which is a manifestation of pulmonary atelectasis, mostly occurring in the posterior part of the lower lobe of the lung. Inclusion effusions tend to occur in the lower part of the chest cavity, either singly or repeatedly, and occasionally in the upper part. On CT image, the encapsulated fluid appears hemispherical or oblate, with an obtuse angle to the chest wall, and the surrounding pleura is uniformly thickened, and its density is significantly higher than that of the fluid, with smooth edges, due to deposits and pleural thickening within the fluid. Fluid flattening is seen in the case of encapsulated liquid pneumothorax. Interlobular effusion can be seen in the relevant parts of the shuttle-shaped liquid density area. Seven, B ultrasound examination A hypoechoic area is visible at the affected area. This examination is simple, mobile, and can be performed at the bedside in severe cases; it has a high diagnostic rate (more than 92%) and can detect pleural effusion below 100mI; it can identify effusion, pleural thickening and intrapulmonary lesions; it can understand the extent of effusion and can be used to locate thoracentesis. Pleural biopsy Pleural biopsy reveals tuberculous granuloma or caseous necrosis to confirm the diagnosis of tuberculous pleurisy, with a positive rate of 71% to 88%, and a positive culture rate of 70% for Mycobacterium tuberculosis in pleural biopsy specimens to facilitate the diagnosis. Due to the low bacteriological detection rate, the diagnosis of tuberculous pleurisy is still made on the basis of a comprehensive understanding of the medical history, clinical symptoms and signs, combined with x-ray performance and laboratory tests. 1, clinical factors causing immune deficiency, varying degrees of fever, cough, respiratory-related chest pain and pleural friction sounds; 2, X-ray examination can be seen (typical or specific) pleural effusion images; 3, the total number of terminal blood leukocytes is normal or high, the sedimentation is fast; PPD skin test is positive or strongly positive; 4, routine laboratory tests of pleural effusion suggest exudate; 5, pleural effusion ADA>45U/L, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit, pleural effusion ADA/hematocrit. Pleural effusion ADA/ serum ADA>l 6.Venous blood CEA is low, generally <10μg/L, pleural effusion CEA/ serum CEA 7.Pleural effusion TB-PCR can be positive; 8.B-type ultrasound examination can be seen in the liquid dark area, which can clarify the scope of effusion and make clinical diagnosis. 9, pleural effusion positive for Mycobacterium tuberculosis (smear, culture, pleural biopsy culture); 10, pleural biopsy can be confirmed by typical tuberculous changes or tuberculous granulomatous changes. In addition to other nature of pleurisy, the diagnosis of tuberculous pleurisy can be confirmed by chest wall pleural biopsy, thoracoscopic biopsy, and even open chest biopsy if the diagnosis is not clear from routine examination. Differential diagnosis Comprehensive clinical manifestations, X-rays and pleural effusion features should be distinguished from the following diseases. Differentiation of exudative pleural effusion (a) Differentiation of tuberculous pleural effusion from cancerous pleural effusion. The onset of tuberculous pleural effusion is mostly under 40 years old (2/3), with urgent onset, fever, chest pain, and moderate amount of pleural effusion, straw yellow and acidic. The disease progresses slowly, and the test of pleural effusion can find Mycobacterium tuberculosis, but the positive rate is low, ADA>45U/L can help the diagnosis, and the pleural effusion is rapidly absorbed after anti-tuberculosis treatment. Cancerous pleural effusion mostly occurs in patients over 40 years of age (2/3), usually without fever, with persistent chest pain, medium to large amount of pleural effusion, alkaline, 50%-90% hematogenous, and cancer cells are found in pleural effusion laboratory for clear diagnosis. Pleural effusion caused by adenocarcinoma has increased carcinoembryonic antigen (CEA). The disease progresses rapidly and is not easily controlled. Pleural biopsy or thoracoscopy is an important tool for the diagnosis of pleural disease. (2) Differentiation between tuberculous pleurisy and purulent pleurisy Purulent pleurisy is secondary to pneumonia, lung abscess, traumatic infection, purulent inflammation of neighboring organs, such as liver abscess in 20%, subphrenic abscess in 80%, and sepsis can also cause purulent pleurisy. The common causative agents are S. pneumoniae, Staphylococcus, Streptococcus and a few bacilli. Purulent pleurisy is characterized by rapid onset, chills, high fever, chest pain and other signs of infection and toxicity, pleural effusion, elevated total leukocyte count, leftward nuclear shift, toxic granules, and purulent pleural effusion; cell count >10X109/L, pus cells can be seen, and pathogenic bacteria can be cultured. Antibiotics and pleural drainage treatment are effective. ( C ) Tuberculous pleurisy and pulmonary schistosomiasis pleurisy about 15% of pulmonary schistosomiasis complicate pleurisy, the disease is associated with raw crab, laguna. The effusion is straw yellow, clear, or milky white, and individually bloody or purulent. The hemorrhagic pleural effusion is eosinophilic, and the pleural effusion can be seen as Charcot-Redden crystals, and occasionally pulmonary schistosome eggs can be found. It is often misdiagnosed as tuberculous pleurisy. A history of living in endemic areas and a positive skin test for pulmonary schistosomes may help in the diagnosis. (iv) Differentiation of tuberculous pleurisy from other rare pleurisy 1. infectious pleurisy such as fungal, actinomycotic, amoebic, etc. 2, connective tissue disease and vasculitis complicating pleurisy such as rheumatoid arthritis 5% occurring pleurisy, mostly in men over 45 years of age, a few occurring before arthritis. Pleural changes can be seen on pleuroscopy, biopsy is non-specific inflammatory granuloma, pleural effusion with sugar <400mg/L, pH<7.20, LDH>700U/L, rheumatoid factor titer>1:320, long-term presence can produce pus or cholesterol chest. Pleural effusion occurs in 50% of SLE with predominantly mononuclear cells, leukopenia, sugar > 600mg/L, pH > 7.35, LDH < 500U/L, antinuclear antibody titer > 1:160, C3 and C4 complement very low, lupus cells can be detected in pleural effusion, etc. 3. It should be differentiated from eosinophilic pleurisy, celiac disease, cholesterol pleurisy, pulmonary embolism reactive pleurisy, etc. Differentiation of leaky pleural effusion 1. Cardiac insufficiency: The pleural effusion in a small number of cardiac insufficiency, especially chronic cardiac insufficiency, can be exudate, which is quite difficult to diagnose clinically. It can be differentiated according to medical history, cardiac symptoms, signs and cardiac function tests. 2.Cirrhosis: Patients with cirrhosis may have pleural fluid due to hypoproteinemia, elevated odd and semichoroidal venous pressure, lymphatic drainage disorders, etc., or abdominal fluid may enter the pleural cavity from the septal orifice, and very few patients have only pleural fluid but no abdominal fluid. Patients with pleural effusion are examined for leaking fluid, accompanied by the performance of the corresponding primary disease, which can be distinguished 3, renal pleural effusion: glomerulonephritis, nephrotic syndrome, uremic syndrome, etc. all cause pleural effusion. Patients with nephrotic syndrome can have a large loss of proteinuria, resulting in hypoproteinemia and decreased colloid osmotic pressure resulting in pleural effusion. It is a part of generalized edema, on both sides, and mostly a fluid at the base of the lungs. Patients with pleural effusion can be differentiated by examination of the leaking fluid with corresponding manifestations of the primary disease [2] X. Disease treatment Tuberculous pleurisy, if left untreated, occurs in about 1/4 of cases, and tuberculosis can occur within 5 months-5 years in some cases with incomplete treatment. Therefore, treatment must be thorough. The objectives of TB pleurisy treatment are: (1) to reduce symptoms and restore lung function; (2) to shorten the course of the disease and restore labor force; (3) to reduce complications and increase the cure rate. Overall, it includes two parts: etiological treatment and local symptomatic treatment. Treatment measures; reasonable chemotherapy and active thoracentesis and aspiration are the basic treatment of tuberculous pleurisy. ( a ) Anti-tuberculosis treatment must follow the treatment principle of “early, combined, regular, appropriate amount and whole course”. The chemotherapy is the same as that for pulmonary tuberculosis, generally using isoniazid (INH), rifampicin (RFP) or rifapentine (RFT-L), pyrazinamide (PZA), streptomycin (SM), and ethambutol (EMB) in combination. Systemic chemotherapy is extremely important to prevent residual Mycobacterium tuberculosis in other parts of the body (intra-pulmonary and extra-pulmonary), since some cases are the result of hematogenous disseminated tuberculosis. The duration of treatment should be 12 months. The intensive period is 2-3 months (4-5 drugs) and the consolidation period is 9-10 months (2-3 drugs). During the treatment period, attention is paid to the adverse effects of the drugs. After 2-3 weeks of treatment, the patient’s body temperature usually returns to normal, and other symptoms of TB toxicity such as general discomfort, night sweats, poor appetite and weakness improve significantly. Timely and adequate treatment is especially important for the healing of tuberculous pleurisy. Timely and adequate anti-tuberculosis treatment can help shorten the course of disease and improve the cure rate. (Active thoracentesis and aspiration can help shorten the course of the disease, prevent pleural hypertrophy and promote the recovery of lung function. The general practice is to perform thoracentesis and aspiration every other day or twice a week until the pleural effusion disappears completely. The recent cure rate is 100% with aggressive aspiration on top of adequate chemotherapy, while the cure rate of chemotherapy alone is only 80% even with very adequate chemotherapy. The occurrence of pleural hypertrophy is inevitably reduced by active aspiration, which is not only related to whether or not to actively aspirate, but also determined by the duration of pleural effusion and the time of starting treatment after the onset of the disease, and the incidence of pleural hypertrophy is inevitably increased by the long duration of the disease and the presence of pleural effusion for too long. Suction of pleural effusion must be accurately positioned to avoid injurious pneumothorax due to fluid extraction. It should be noted that the speed of aspiration should be slow, and the amount of aspiration depends on the amount of fluid and the patient’s adaptability to aspiration, generally no more than 1500 ml of fluid should be aspirated each time. Once the patient becomes irritable, pale, sweating, blood pressure decreases and other uncomfortable reactions, the pumping should be stopped immediately and the patient should be placed in a flat position, and the patient can recover after a few moments of rest. (Adrenal corticosteroids are not routinely used in the treatment of tuberculous pleurisy. Whether to add adrenocorticotropic hormone to the treatment of tuberculous pleurisy is determined by the condition. The main beneficial effect of adrenocorticosteroids on tuberculous pleurisy can be achieved by active chemotherapy and active pleural fluid aspiration, and in some cases when adrenocorticosteroids are discontinued, there is a rebound in body temperature or pleural fluid that prolongs the course of the disease, and there is no definite effect on preventing pleural thickening. The rational chemotherapy and active thoracentesis and aspiration have been effective in preventing pleural thickening. Since adrenocorticotropic hormone can promote the absorption of pleural effusion, reduce the symptoms of tuberculosis poisoning and shorten the course of the disease, adrenocorticotropic hormone can be applied early. Adrenocorticosteroids can be used in the following cases of tuberculous pleurisy: (1) cases with particularly severe clinical symptoms of massive pleural effusion; (2) cases with multiple plasmacytosis; (3) cases with complicated hematogenous pulmonary tuberculosis; and (4) cases of pleural effusion not easily punctured (e.g. interlobular effusion). Prednisone is usually started at 30-40mg/d (once daily) in the morning. The dosage is gradually reduced after the pleural effusion is obviously absorbed, and the dosage is gradually reduced by 5-10mg per week, and the drug is usually stopped in 4-6 weeks. If the dose is reduced too quickly or for too short a period of time, pleural effusion or rebound of tuberculosis toxicity symptoms may easily occur. It is no longer used in cases of existing pleural thickening or chronic tuberculous pleurisy. (iv) Intrathoracic administration 1, anti-tuberculosis drugs Tuberculous pleurisy can be treated by aggressive anti-tuberculosis chemotherapy and aggressive fluid extraction, and no anti-tuberculosis drugs need to be given in the chest cavity. For chronic tuberculous pleurisy with a tendency to abscess and encapsulated pleural effusion cases can be administered in the chest cavity. Generally, after flushing the chest cavity with 2% bicarbonate (the amount of flushing fluid should not exceed 500ml), the chest cavity should be injected with anti-tuberculosis drugs such as isoniazid (INH) 0.1-0.3g, amikacin (Am) 0.2-0.4g, or INH 0.1g, RFP 0.15g-0.3g; 1-3 times a week, after thoracentesis and fluid extraction. 2. Intrathoracic injection of fibrinolytic enzymes streptokinase (SK) and urokinase (UK) can effectively reduce the thin fibrin adhesions in tuberculous pleurisy, but is less effective in thicker fibrin layers or mechanized fibrous plates. Urokinase has fewer side effects than streptokinase and is commonly used in clinical practice. ( V ) Other treatments The literature reports that thoracoscopic treatment of tuberculous recalcitrant pleural effusion has achieved good results. ( VI ) Treatment of encapsulated tuberculous pleurisy Intrapleural administration of drugs such as INH, SM, KM, RFP, one or two of them, 3 times / week. If the treatment effect is not good, surgical treatment can be considered according to the size of the encapsulated fluid and the amount of fluid accumulation. ( VII ) Treatment of interlobular pleurisy Interlobular pleurisy pleural aspiration is difficult, add adrenocorticotropic hormone under reasonable chemotherapy, the usage is the same as that of exudative pleurisy. If ultrasound can be localized, try to aspirate as much fluid as possible. Surgical treatment may be considered for those who cannot be absorbed after active treatment. (H) Chinese medicine treatment Tuberculous pleurisy with toxic side effects, gastrointestinal discomfort, and resistance to western drugs can be treated with Chinese medicine. Chinese medicine is a dialectical treatment to support and strengthen the root, improve the patient’s own immunity, and alleviate the side effects produced by western chemotherapy. Eleven, disease prognosis Tuberculous pleurisy can be cured after anti-tuberculosis and pleural fluid pumping treatment, while it should be noted that 30% can develop tuberculosis within five years, and must adhere to the full and regular anti-tuberculosis treatment, otherwise it may also relapse. In case of recurrent tuberculous pleurisy with poor efficacy and persistent chest pain, we should be alert to the possibility of pleural carcinoma. Twelve, dietary attention (a) diet should be rich in nutrition, it is appropriate to eat a high protein, high vitamin diet, to eat more vegetables and fruits containing vitamins. Protein-rich foods include: animal foods, such as chicken, duck, goose, lean pork, beef and mutton; plant foods, such as flour, bean foods and soybean products, which should be cooked and rotten when consumed, and should not be raw and indigestible, which is not conducive to human absorption. (B) avoid spicy food. (C) have a habit of smoking and alcohol should be firmly quit. (D) Try to eat less or no seafood, because anti-TB drugs have the side effect of increasing blood uric acid, and seafood will aggravate the effect of increasing blood uric acid. (v) Take anti-TB drugs on time and in the right amount every day, and recheck the blood routine and liver and kidney functions in about 7-14 days. (6) Pay attention to rest, strengthen nutrition, regulate immunity, and avoid getting cold; (7) Anti-tuberculosis treatment should be standardized, and the medication should be used in sufficient quantity and duration under the guidance of doctors, and should not be stopped prematurely, and the general course of treatment should be about 9-12 months to avoid the occurrence of distant intrapulmonary and extrapulmonary tuberculosis, or the possibility of relapse when the body’s resistance decreases. Care for the disease (a) Avoid wind and cold, be cautious in your daily life, enjoy your mood, stop smoking and drinking, and do not eat cold and raw food. (2) If there is fever, give antipyretic treatment. Observe the relationship between chest pain and coughing and breathing. If the chest pain increases when coughing and breathing, avoid too much lateral turning to increase the pain. For massive fluid accumulation and respiratory difficulty, take a semi-recumbent position and give oxygen as appropriate. (C) Have pleural effusion to be promptly pumped, and pay attention to observation of breathing and heart rate after pumping. (iv) Life and living should be regular, and it is best to take a full rest for 2-3 months according to the condition, and then arrange work appropriately. Be careful not to be overly fatigued. Usually, you should keep your spirit relaxed, happy, and appropriate physical exercise. (E) Diet should be light and nutritious. When the amount of fluid is too much, a vegetarian semi-fluid diet is appropriate. When fluid accumulation decreases, it is advisable to gradually increase milk, eggs, lean meat and other nutritious foods. (f) When the disease tends to improve, the amount of activity can be gradually increased, but do not overwork. Complications (a) If exudative pleurisy is not treated timely or improperly, it will quickly develop into encapsulated effusion. (ii) Improper treatment of simple tuberculous pleurisy or failure to complete the prescribed course of treatment results in the development of other sites of tuberculosis or severe tuberculosis, such as disseminated tuberculosis, pulmonary tuberculosis, and chest wall tuberculosis, in about 2/3 of patients within 5 years. (iii) Tuberculous pneumothorax can be caused when intrapulmonary cavities and case-like lesions break down near the pleural area. (d) Pleural fluid of exudative pleurisy, if not treated in time, can also gradually caseinate or even become purulent and become tuberculous pneumothorax. (e) Pleural hypertrophy on one side of the formation of fibrous plate bound lung function can be complicated by emphysema on the opposite side, which can also lead to chronic pulmonary heart disease, and even cardiopulmonary failure. Fifteen, expert opinion 1, tuberculous pleurisy after a clear diagnosis to regular anti-tuberculosis treatment, the course of treatment is generally about 12 months. 2, in the early stage of the disease, there is pleural effusion, can actively pumping pleural fluid treatment, 2-3 times a week or perform thoracic intubation, drainage of fluid, but pay attention to the first release of fluid can not be too fast, the amount generally does not exceed 1000ml. 3, there is high fever, chest tightness, cough and other symptoms to timely symptomatic treatment. 4.During anti-tuberculosis treatment, blood routine and liver and kidney function should be rechecked monthly, and chest X-ray or CT examination should be performed in 2-3 months. 5.If an encapsulated pleural effusion is formed, which affects lung function, surgical operation can be considered after 6 months of anti-tuberculosis treatment. 6.If a tuberculous abscess chest or bronchopleural fistula is formed, surgical treatment can be considered. 7.For difficult to control pleural effusion, other diseases should be excluded, consider whether there is a possibility of drug resistance, do culture of tuberculosis bacteria and drug sensitivity test, and adjust anti-tuberculosis drugs.