1.Etiology Pus accumulation in the pleural cavity due to tuberculosis infection forms tuberculous abscess chest. Often due to the diagnosis, treatment delayed for a long time, easy to become chronic pus chest. Most of the ways of invasion of tuberculosis infection into the pleural cavity are through tuberculosis lesions in the lung. Some tuberculosis lesions are at the edge of the lung, close to the pleura, which are easily eroded by tuberculosis; some lesions rupture and enter the pleural cavity in large quantities together with air and tuberculosis bacteria, producing spontaneous pneumothorax and bronchopleural fistula. Tuberculosis of the spine or chest wall may also invade the pleural cavity. In addition, tuberculosis bacteria may also invade the pleura via lymphatic or blood circulation, causing infection; or post-operative complications of tuberculosis artificial pneumothorax, contamination of the chest cavity during tuberculosis surgery, etc. and lead to tuberculous abscess chest. 2.Pathology At the early stage of tuberculous abscess chest, the pleura becomes congested, edematous and exudate. Tuberculous nodules may be formed. The pleural fluid is plasma, containing white blood cells and fibrin, and after a longer period of time, the plasma fluid in the pleural cavity gradually becomes purulent fluid and becomes pus. If the lung lesion is ruptured or punctured with other bacterial infection, a thick and solid layer of fibrous plate is formed. And there is often calcification. The pus thorax may be limited or total. The fibrous layer of scar mechanization shrinks, narrowing the intercostal space, sinking the chest wall, triangular-shaped ribs, atrophy and fibrosis of the intercostal muscles, and protrusion of the spine to the opposite side. Sometimes the pus collapses out from the intercostal space and becomes a self-flushing abscess, forming a cold abscess in the chest wall or breaking down into a sinus tract, which does not heal for a long time. 3.Clinical manifestation and diagnosis The symptoms of tuberculous abscess chest are very inconsistent. Generally, it starts slowly and may have symptoms such as low fever, night sweats, mild chest pain, chest tightness, dry cough, weakness and wasting. Toxic symptoms are more pronounced because of the strong absorption capacity of the pleura in the early stage. The presence of active tuberculosis lesions in the lungs may also produce symptoms of varying degrees. If pleural effusion is high, shortness of breath and dyspnea may occur. If there is a bronchopleural fistula, there may be an irritating cough, and the cough is position-dependent. If the patient is lying on the healthy side, the cough is frequent, and the cough produces the same purulent sputum as the pleural fluid, sometimes with hemoptysis, and often with dyspnea. When there is secondary infection, the symptoms are the same as those of acute pustulothorax. If tuberculosis is disseminated due to bronchopleural fistula, the condition will be more serious. Tuberculous pustulothorax starts slowly, and the patient has symptoms of tuberculosis poisoning and mostly tuberculous lesions in the lungs. Thoracentesis may extract thin pus or pus containing cheese-like material. The diagnosis is established by detecting Mycobacterium tuberculosis in the pleural puncture fluid, but it is not easily detected in most patients. The positive rate of pleural fluid is very low, and any pleural fluid with many lymphocytes and negative pus culture should be first considered as a tuberculous pustule. In patients with pulmonary tuberculosis who have a history of receiving artificial pneumothorax treatment, the possibility of tuberculous abscess chest is higher. x-ray examination can reveal the pus accumulation and the condition of both sides of the lung, but cannot determine the nature of the abscess chest. In the presence of a large fluid collection, intrapulmonary lesions are often obscured. If a bronchopleural fistula is present, the fluid plane is visible on chest radiography or fluoroscopy. This can be confirmed if the patient coughs up stained sputum after intrapleural injection of methylene blue or methyl violet. The diagnosis can be further confirmed if tissue from the wall of the abscess cavity can be excised for pathological examination. However, due to the application of anti-tuberculosis drugs and local tissue repair, the pleural biopsy of some cases of tuberculous abscess chest may not necessarily show typical specific tuberculosis pathological changes, but only “chronic inflammation” pathological characteristics, or fibrous scar tissue. In this kind of cases, the clinic cannot exclude tuberculous pustulosis, and should make a comprehensive judgment to make a correct diagnosis. 4.Treatment Adequate anti-tuberculosis treatment in the early stage. It can prevent the occurrence of tuberculous abscess chest. After the occurrence of abscess chest, the treatment is basically the same as that of chronic abscess chest, but it should also be actively treated with anti-tuberculosis drugs. In early plasmacytic exudation, rest and nutrition therapy are used. The drugs are used in combination with isoniazid, rifampin and ethambutol, which can mostly be absorbed by themselves. When there is a large amount of exudative pleural fluid, thoracentesis can be done to extract fluid, but care should be taken to prevent secondary infection. After the occurrence of secondary mixed infection, active drainage and antibiotics should be added. If the above drugs are not cured for a long time, surgical treatment needs to be considered. The method of surgical treatment is the same as that of chronic abscess chest.