(I) Etiology
Acute abscess chest is diagnosed too late, not treated in time, not timely thoracentesis or closed drainage of the chest, gradually turned into chronic abscess chest. Improper treatment of acute abscess chest, such as drainage tube is too thin, positioned too high, placed too deep, too shallow, or distorted, resulting in poor drainage and residual pus, gradually turning into chronic abscess chest. The presence of foreign bodies in the abscess cavity, such as shrapnel, dead bone, cotton balls, and drainage tube stumps, makes it difficult to control the infection in the pleural cavity.
Combined bronchial fistula or esophageal fistula without timely treatment. Infected foci in adjacent organs: liver abscess, subdiaphragmatic abscess, rib osteomyelitis, etc. repeatedly introduced infection, resulting in failure to close the abscess cavity. The presence of special pathogenic bacteria, such as tuberculosis, actinomycetes and other chronic inflammation causing chronic abscess chest.
(II) Pathology
The pathological changes of chronic abscess chest are in the mechanized stage. Due to long-term accumulation of pus in the pleural cavity, the fibrous layer of the pleura is mechanized to form a hard fibrous plate. The thickening of the fibrous plate of the dirty layer is relatively thin, while the thickening of the fibrous plate of the wall layer is relatively thick, mostly 0.2~1.6cm or thicker.
In chronic septic chest, the pleural fibrous plate is thickened to a considerable extent and also calcified extensively, forming a hard bony fibrous plate. The contracture of the pleural fibrous plate in chronic septic chest causes intercostal narrowing, thoracic inversion, and curvature of the spine to the opposite side, thus severely restricting the movement of the thorax. The visceral pleura and lungs are restricted by the encapsulation of the mechanized fibrous plates, which affects the respiratory movements of the lungs and also restricts the diastole of the lungs. The diaphragm is also limited by the thickened fibrous plates. The mediastinum, on the other hand, is contracted by the fibrous plates and tractionally displaced to the affected side. Some patients may develop pestle-like fingers (toes) due to long-term chronic hypoxia. A few patients with chronic abscess chest for many years have extensive calcification of pleural fiberboard into hard bony fiberboard, resulting in extensive ossification in the thorax, fixation of mediastinum, partial fusion of rib bones, and severe atrophy and even ulceration of lung.
Patients with chronic abscess chest have long-term infection and amyloidosis of liver, kidney, spleen and other organs, with hepatomegaly, splenomegaly and abnormal liver and spleen functions. In a small number of chronic abscess chest, pus penetrates the pleura through the intercostal space and forms a dumbbell-shaped abscess, which becomes an external penetrating abscess chest.
(III) Clinical manifestations
Due to long-term infection and chronic consumption of chronic abscess chest, patients have systemic toxic symptoms such as hypothermia, weakness, loss of appetite, emaciation, malnutrition, anemia and hypoproteinemia. Signs include shortness of breath, cough, and pus sputum production. There is thoracic inversion, narrowing of the rib space, decreased or absent respiratory dynamics, mediastinal displacement to the affected side, scoliosis, and pestle-like fingers (toes). The percussion sounds are solid, and the breath sounds are diminished or absent on auscultation.
X-ray chest film shows thickening of the pleura, narrowing of the rib space, and a blurred glassy shadow with increased density. The diaphragm is elevated, the mediastinum is shifted to the affected side, and the spine is scoliosis. High-voltage x-ray of the chest reveals thickened pleura, the size of the abscess cavity, and compression and atrophy of the lung. If there is a fluid plane suggesting a bronchopleural fistula. If there are sinus tracts or chest drains in the chest wall, iodine oil or 12.5% sodium iodide can be injected to create an image, and frontal and lateral X-ray chest films can be taken to clarify the site and size of the abscess cavity and the presence of bronchopleural fistula. The extensive ossification in the thorax can be clearly shown.
If chronic abscess chest has not been drained, thoracentesis should be done to extract pus for bacterial culture and drug sensitivity test to clarify the causative organism of abscess chest and select effective antibiotics.
(IV) Diagnosis
According to the symptoms, signs, X-ray examination and CT scan of chronic abscess chest and the pus extracted by thoracentesis, a clear diagnosis can be made. If there is bronchopleural fistula, the sputum produced by the patient is the same as the pus extracted by thoracentesis, and the patient produces blue sputum by injecting methylene blue into the pus cavity. In chronic abscess chest that has been drained, if there is no bronchopleural fistula, saline can be injected into the abscess cavity through the drainage tube to measure the size of the abscess cavity. To find the cause of chronic abscess chest, chronic abscess chest mostly has a history of acute abscess chest, chest trauma or chest surgery, and pus culture can find pathogenic bacteria. Tuberculous pustules mostly have a history of tuberculosis, the pus often has cheese-like material, and the pus culture can find Mycobacterium tuberculosis. Amoebic pustules often have a history of amoebic dysentery or liver abscess, the pus is coffee-colored, and amoebic trophozoites can be found. With a history of chest trauma or chest surgery, pus culture can find pathogenic bacteria.
(V) Treatment
Chronic abscess thorax mostly requires surgery due to the change of pathological anatomy. The principles of treatment for chronic abscess chest are: to improve systemic symptoms; to eliminate the causative agent and pus cavity; to promote lung reopening and restore lung function.
1.Systemic treatment
2.Improve chest drainage
3.Open flap surgery
4.Pleural fiber plate stripping
5.Thoracoplasty
6.Pleuropneumonectomy