A few common questions about septic chest

  Pleural cavity is infected by purulent pathogens and produces purulent exudate accumulation, which is called abscess thorax. According to the extent of the lesion, it is divided into total and limited abscess thorax. Total abscess pleura means that pus occupies the entire pleural cavity, and limited abscess pleura means that pus accumulates between the lung and chest wall or between the transverse or mediastinal septum, or between the lobes of the lung and the lobes of the lung, also known as encapsulated abscess pleura.
  Most of the abscess thorax is secondary, and the pathogen comes from infection in the thoracic cavity or in the organs or tissue spaces near the thoracic cavity, such as bacterial pneumonia, bronchial dilatation infection, lung abscess rupture or liver abscess, subdiaphragmatic abscess, mediastinal abscess, renal abscess rupture penetrating into the thoracic cavity, etc. Thoracic infection caused by post-surgery and thoracic trauma is also the cause of abscess chest. According to the different pathogens, it can be divided into non-specific and specific abscess chest. General bacterial infection is non-specific pustulothorax, while tuberculosis or amoebic protozoal infection is specific pustulothorax, which can also be directly called tuberculous pustulothorax or amoebic pustulothorax. The pus caused by mixed strains of infection including anaerobic bacteria is dark gray, thick and foul-smelling, which is called corrosive pustulothorax. The course of the disease within 4-6 weeks is acute pustulothorax, and the early stage is dominated by a large amount of exudate, which is called the exudative stage. In this period, if the exudate is removed and the infection is controlled, the abscess chest can be cured and the lung can be well reopened. If the exudate is not cleared and a large amount of fibrin is deposited, the fibrin membrane is formed and enters the fibrous septic phase, and then the fibrin membrane is mechanized to form a fibrous plate and calcified, the septic chest enters the mechanized phase, which is chronic septic chest. For early encapsulated abscess chest, thoracoscopy is feasible to open the separation, remove the fibrous membrane on the lung surface and accurately place the drainage tube. Nutritional support therapy can improve the nutritional status of the body and increase the resistance of the body. If acute abscess chest is not treated timely, appropriately or thoroughly, it will turn into chronic abscess chest. In chronic abscess pleura, the pleura is highly thickened to form a fibrous plate, mechanized and fixed, the thorax is collapsed, the rib space is narrowed, the lung activity is restricted, and the lung function is seriously affected. The consumption of large amount of pus formation and continuous fever makes the patient present a depleted condition, and the severe cases show cachexia. Chronic abscess thorax is treated by surgical treatments such as fibrous plate resection, pleuropneumonectomy or thoracoplasty, tipped greater omentum filling, pectoralis major muscle flap or latissimus dorsi flap filling, etc. Thoracoscopy or thoracoscopy-assisted small incision pleural fibrous plate debridement is currently the main treatment for chronic abscess thorax in our department to eliminate the causative factors and close the abscess cavity, but preoperative systemic support therapy must be applied to improve the systemic condition, correct negative nitrogen balance and restore the hydroelectric balance.
  Etiology and pathogenesis
  1.Pulmonary infection
  About 50% of acute abscess chests are secondary to inflammatory lesions in the lungs. Pulmonary abscess can directly invade the pleura or rupture to produce acute abscess thorax.
  2.Purulent lesions in adjacent tissues
  Mediastinal abscess, subdiaphragmatic abscess or liver abscess, the pathogenic bacteria invade the pleural cavity through lymphatic tissue or direct penetration, which can form unilateral or bilateral abscess chest.
  3.Thoracic surgery
  Postoperative pus chest mostly occurs in combination with bronchopleural fistula or esophageal anastomotic fistula. A smaller part is due to intraoperative contamination or postoperative incision infection penetrating into the chest cavity.
  4.Thoracic trauma
  After chest penetrating injury, the pathogenic bacteria can be brought into the pleural cavity due to foreign bodies such as shrapnel and clothing debris, which, together with the frequent hemothorax, can easily form septic infection.
  5.Sepsis or septicemia
  Bacteria can reach the pleural cavity through the blood circulation to produce pus, which is mostly seen in infants and children or weak patients.
  6.Other
  Such as spontaneous pneumothorax, or other causes of pleural effusion, after repeated puncture or drainage complications of infection; spontaneous esophageal rupture, mediastinal teratoma infection, penetration into the thoracic cavity can form abscess chest. Second, the pathophysiology of pleural cavity infection with bacteria first causes congestion, edema, exudation, loss of luster and lubricity of the pleura in the dirty layer and wall layer. The exudate contains polymorphonuclear neutrophils and fibrin, which is thin and clear at the beginning and gradually becomes cloudy in appearance due to the increase of fibrin and pus cell formation, and finally becomes pus whose volume increases rapidly, causing atrophy of the lung under pressure and pushing the mediastinum to the opposite side, resulting in respiratory and circulatory disorders. If there is bronchopleural fistula or esophageal anastomotic fistula, tension pneumothorax can be formed, and the effect on respiratory and circulatory function is more obvious. At the same time, fibrin deposited on the surface of dirty and wall pleura, forming fibrous membrane, which is soft and brittle at the beginning, but as the pus thickens, the fibrous membrane gradually becomes mechanized, thickens and becomes tougher, forming fibrous plate, fixing and compressing lung tissue, and limiting lung expansion. Pleural cavity infection is widespread, the area expands, and the whole pleura is involved in the development of a full septic chest. If the infection is more limited or the drainage is incomplete and adhesions are formed around it, so that the pus is confined to a certain area, it forms a confined or encapsulated septic chest, which is commonly located in one or more places such as between the lobes of the lung, above the diaphragm, the posterior and lateral parts of the pleural cavity and the mediastinal surface. The pressure on the lung tissue and mediastinum is not as serious as that of total septic chest, and the respiratory and circulatory function is also less affected than that of total septic chest. Before the widespread use of antimicrobial agents, the causative agents of pneumococcus and streptococcus were mostly pneumococci, but later on, Staphylococcus aureus was the main cause, and 92% of pneumothorax in children under 2 years old were such infections. In cases of combined bronchopleural fistula, the abscess chest mostly has mixed infections, such as anaerobic bacterial infection, which is corrosive and purulent, and the pus contains necrotic tissue and has a foul odor. Pulmonary tuberculosis involving the pleura or having cavity rupture can form a tuberculous abscess chest.
  Diagnosis
  To confirm the diagnosis of abscess thorax, thoracentesis must be done to extract pus. Smear microscopy, bacterial culture and antimicrobial susceptibility test should be performed, and effective antimicrobial treatment should be selected accordingly. On examination, we can see a feverish face, sometimes unable to lie down, reduced fibrillation on the affected side of the chest, turbid sounds and percussion pain on percussion, and reduced or absent breath sounds on auscultation. White blood cell count is increased, neutrophils increase to more than 80%, and there is a left shift of the nucleus. Chest x-ray examination varies depending on the amount and location of pleural fluid. A small amount of pleural effusion can be seen as a faint shadow of disappearing sinus of the rib diaphragm; when the amount of effusion is large, the lung tissue can be seen to be compressed and atrophied, and the effusion is an arc-shaped shadow of high external and low internal; a large amount of effusion makes a uniform faint shadow on the affected side of the chest, and the mediastinum is displaced to the healthy side; when the effusion is confined to the lobe of the lung, or located between the lung and mediastinum, diaphragm or chest wall, the confined shadow does not change with the change of position, and the edge is smooth, and sometimes it is not easily distinguished from pulmonary atelectasis. Sometimes it is not easily distinguished from atelectasis. In cases of bronchopleural fistula or esophageal anastomotic fistula, gas-fluid planes are seen.
  Treatment
  The treatment principles of acute abscess chest include infection control, pus removal and systemic support treatment.
  1.Control of infection: select effective and sufficient amount of antimicrobial agents according to the pathogenic bacteria and drug sensitivity test, take intravenous administration as the best, observe the efficacy and adjust the drugs and dose in time.
  2.Exclusion of pus: It is the key to the treatment of abscess chest. Infants and children under one year old can be treated by puncture and intrathoracic injection of antimicrobial agents, and more satisfactory results can be obtained. For older patients, closed drainage of the chest cavity should be performed as early as possible to drain the pus and promote early expansion of the lung, and attention must be paid to the selection of drains of suitable texture and caliber to ensure smooth and effective drainage. If the pus is thick, a thick drainage tube should be placed, and it is forbidden to use a catheter to drain the pus. The correct site for drainage is the lowest part of the pus cavity, usually the 7th intercostal space in the posterior axillary line, and if it is encapsulated, it should be positioned well under x-ray or ultrasound before drainage. A 3-5 cm long section of rib is removed under local anesthesia, and the periosteum and mural pleura are cut after the pus is extracted by puncture, and the drainage tube is placed about 3 cm deep after the finger is inserted into the pus cavity to determine the appropriate site, and the soft tissue and skin around the drainage tube are tightly sutured to prevent air leakage. Regular postoperative x-ray examination was performed to adjust the chest drainage tube at any time; to ensure unobstructed drainage and encourage the patient to move to the floor more often. Record the drainage flow daily for comparison. If the pus is sticky, a thin plastic tube with a caliber of 2-4 mm can be placed into the lumen through the hole in the wall of the drainage tube to reach the pus cavity, and 500 ml of 2% methotrexate or sterile physiological saline can be dripped into this tube for flushing every day, which can not only dilute the pus to facilitate drainage but also keep the drainage tube open. After two weeks of drainage, sterile saline can be used to measure the pus cavity, and then once a week, when the pus cavity shrinks to less than 50 ml, the drainage tube can be cut and changed to open drainage, until the pus cavity shrinks to about 10 ml, the thin tube can be replaced, and gradually cut short until complete healing.
  3.Systemic supportive treatment: It should include giving high protein, high calorie and high vitamin diet, and encouraging more water intake. If necessary, intravenous rehydration and blood transfusion.