The early stage of pleural infection by tubercle bacilli mainly shows pleural congestion and edema, followed by serous or slightly turbid straw-yellow plasma exudate. With further development of inflammation, the exudate increases in organic fractions (fibrin, inflammatory cells, tuberculosis bacilli) and slowly turns into cloudy plasma pus or purulent fluid, the pus gradually thickens, and the fibrin within the pus gradually settles on the pleura, which later mechanizes into fibrous tissue. This fibrous layer wraps around the lung and prevents the expansion of the lung, and the longer it takes, the thicker or even calcified the fibrous layer becomes. There is a layer of loose connective tissue between the fibrous layer and the dirty pleura, and tuberculosis infection is often limited to the inner part of the fibrous layer, rarely invading the whole fibrous layer, so it is possible to perform fibrous layer debridement. After this layer is removed, the compressed lung can still be reopened. However, the lung tissue that has been compressed for a long time often has fibrous sclerosis, distortion, dilatation or narrowing of the bronchi, or even secondary infection, and the lung cannot be satisfactorily expanded despite removal of the fibrous layer. If the tuberculous lesion of the lung causes loss of connective tissue between the fibrous layer and the dirty pleura, and if it is extensive, it is naturally not possible to perform such fibrous layer debridement. The fibrous layer of the wall pleura proliferates rapidly, and with time and fibroblast proliferation, the fibrous plate of the wall layer is much thicker than the fibrous plate of the dirty layer, even reaching more than 3 cm, and is hard, lacks blood flow, is grayish in color, and often has flaky calcifications. The contraction of the fibrous scar causes the thorax to sink, the rib space to narrow, the ribs to be triangular in shape with their bases facing outward, and the intercostal muscles to atrophy and fibrosis. The diaphragmatic pleura and mediastinal pleura are held in place by thickened fibrous plates, causing the mediastinum to shift to the affected side and eventually scoliosis to the healthy side. If the pleural cavity inflammation involves the whole pleural cavity, it is total abscess chest; if it involves part of the pleural cavity and there are adhesions and wrapping formation, the accumulation of pus in single or multiple rooms is limited abscess chest (or wrapped abscess chest). Restricted abscess thorax can occur in any part of the thoracic cavity and is common in the lateral part. However, confined abscess thorax in interlobular, mediastinal and supra-diaphragmatic areas poses some difficulties in diagnosis and management. Abscess thorax is usually mostly unilateral, and bilateral is also seen. Wang Cheng, Department of Thoracic Surgery, Shandong Provincial Chest Hospital
Chronic tuberculous abscess chest accumulates a large amount of pus in the abscess cavity during the long-term course of the disease, and the wall of the abscess cavity is born with a large amount of granulation and cheese necrosis (a large amount of accumulation at the bottom of the abscess cavity). If proper treatment is not obtained for a long time, it often penetrates into the lung tissue or chest wall to form a bronchopleural fistula or chest wall fistula, making the tuberculous abscess chest a mixed abscess chest. The pus becomes thicker and smells foul, causing extensive and repeated dissemination to both lungs; the chest wall fistula overflows with pus and does not heal, and even if the fistula opening heals after natural drainage, it re-rupts when the body’s resistance is low or when there is a lot of pus in the chest cavity. When there is a large amount of granulation in the pus cavity, the granulation is very easy to bleed (especially hemolytic pyogenic infection), forming a pus and hemothorax. Due to serious bleeding and accumulation of large amount of corrosive blood clots and blood in the abscess cavity, the pressure inside the abscess cavity is very high, which seriously endangers the patient’s life.
Suppurative chest with bronchopleural fistula or chest wall fistula, which allows gas to enter the abscess cavity and become pneumothorax. Pneumothorax caused by tuberculous cavity, postoperative bronchopleural fistula, etc. is mostly tension pneumothorax. Pus pneumothorax caused by chest wall fistula is open pneumothorax. These pneumothoraxes are often accompanied by severe mixed infections. At the same time, the lung tissue is severely atrophied and the mediastinum is severely displaced, thus causing acute severe impairment of respiratory and cardiovascular functions.
In chronic tuberculous pneumothorax, due to long-term chronic chest infection or chronic hypoxia, tissue hyperplasia is formed, and patients can see pestle-like fingers (toes), the ends of the fingers (toes) are inflated like a mallet, and the longitudinal and transverse backs of the nails are highly curved like glass-like changes. Patients with chronic tuberculous septic chest may have amyloid changes in their liver, kidney, spleen and other organs due to long-term consumption and poisoning. The liver and spleen are enlarged, the kidney function is reduced, and even protein, red and white blood cells or tubular patterns can be detected in the urine.