Spontaneous pneumothorax can be divided into two types according to whether there is primary disease or not: primary pneumothorax and secondary pneumothorax.
The factors that induce pneumothorax are strenuous exercise, cough, lifting heavy objects or holding the upper arm high, lifting weights, and difficulty in defecation. When coughing violently or defecating forcibly, the pressure in alveoli rises, which breaks the damaged or defective lung tissue and causes pneumothorax. When using artificial respirator, pneumothorax may occur if the air supply pressure is too high. According to statistics, 50% ~ 60% cases have no obvious inducement, and about 6% patients are even bedridden.
1. Primary pneumothorax, also known as idiopathic pneumothorax, refers to a pneumothorax in which no obvious pathological changes can be found by routine X-ray examination of the lungs of healthy people, and it is prone to young people, especially slender men. According to foreign literature, this kind of pneumothorax ranks first in spontaneous pneumothorax, while secondary pneumothorax is the main one in China.
The etiology and pathological mechanism of the disease are still unclear. Most scholars believe that it is caused by the rupture of subpleural microbubbles and pulmonary bullae. According to the pathological examination of pulmonary bulla in patients with idiopathic pneumothorax, it is found that it is based on non-specific inflammatory scar under pleura, that is, non-specific inflammation around bronchioles makes elastic fibers and collagen fibers in visceral pleura and subpleural pleura proliferate and form scars. It can reduce the elasticity of adjacent alveolar walls, lead to alveolar rupture and form pulmonary bullae under pleura. Nonspecific inflammation of bronchioles itself acts as a one-way valve, which changes interstitial or alveolar emphysema and forms pulmonary bullae.
Some scholars believe that congenital hypoplasia of lung tissue is the cause of bullae formation, that is, elastic fibers are congenital hypoplasia, but their elasticity is low, and alveolar walls expand to form bullae and rupture. Marfan syndrome (a congenital connective tissue deficiency) is a typical example of spontaneous pneumothorax. There are reports of familial spontaneous pneumothorax abroad, and 725 cases of spontaneous pneumothorax reported in Miyagi have 1 1 family history.
Among the causes of this disease, some people put forward the theory of "new membrane", the mechanism of collateral ventilation disorder and the theory of air pollution.
2. Secondary pneumothorax is caused by the formation of pulmonary bullae or direct injury to pleura on the basis of other lung diseases. It is often caused by chronic obstructive emphysema or inflammatory fibrosis (such as silicosis, chronic tuberculosis, diffuse interstitial fibrosis, cystic pulmonary fibrosis, etc.). ). Bronchiolitis is narrow and twisted, leading to the formation of pulmonary bullae valve mechanism. Swelling emphysema degenerates due to nutritional and circulatory disorders. Cough, sneezing or increased pressure in the lungs can lead to rupture of pulmonary bullae and pneumothorax. In 179 cases of spontaneous pneumothorax reported by Wu et al., chronic bronchitis with emphysema accounted for the first place (38.5%), followed by tuberculosis (17.3%), idiopathic pneumothorax (13.4%) and staphylococcus aureus pneumonia (65433).
Septic pneumonia caused by Staphylococcus aureus, anaerobic bacteria or Gram-negative bacteria, rupture of lung abscess to chest cavity, lung infection caused by microorganisms such as empyema, fungi or parasites, pneumothorax caused by infiltration or puncture of visceral pleura, and rupture of bronchial pulmonary cyst. In addition, pneumothorax can also be caused by perforation of adjacent organs such as esophagus into pleural cavity, application of positive pressure artificial ventilation and long-term use of glucocorticoid.
In recent years, people have gradually paid attention to the secondary pneumothorax caused by some diseases:
① Lung cancer, especially metastatic lung cancer, with the progress of comprehensive treatment, the survival time of lung cancer patients is gradually prolonged, and the secondary pneumothorax of lung cancer is bound to increase day by day; Its incidence accounts for 4% of lung cancer patients (especially advanced small cell lung cancer). The reasons are as follows: (1) The tumor blocks bronchioles, leading to localized emphysema; Obstructive pneumonia further developed into pulmonary suppuration and finally broke into the chest cavity; The tumor itself invades or destroys the visceral pleura,
② Sarcoidosis, mainly in the third stage, and the incidence of pneumothorax is 2% ~ 4%, which is caused by the formation of subpleural bullae or granulomas in the later stage of fibrosis directly invading the pleura.
③ Histiocytosis X: It is reported that the incidence of spontaneous pneumothorax can reach 20% ~ 43%, which is related to obvious pulmonary fibrosis in the late stage of the disease, eventually leading to "honeycomb lung" and forming pulmonary bullae.
④ Pulmonary lymphangioleiomyomatosis (LAM): According to literature reports, about 40% patients are complicated with spontaneous pneumothorax. Taylor reported that among 32 cases of LAM, 26 cases (865,438 0%) had pneumothorax, which was closely related to the changes of estrogen in the body. Parabronchial smooth muscle hyperplasia can partially or completely block the airway, leading to pulmonary bullae and pulmonary cyst, and finally leading to rupture and pneumothorax.
⑤ AIDS: The incidence of spontaneous pneumothorax is 2% ~ 5%. Coker et al reported that the incidence of pneumothorax was 4% among 298 AIDS patients. Its mechanism may be: the disease is easy to invade pleuropneumonia, and it is easy to be complicated with pneumocystis carinii pneumonia, which has destructive effects on lung and pleura and leads to pneumothorax; The direct cytotoxicity of human immunodeficiency virus (HIV) located on pulmonary macrophages causes the release of elastase, which leads to emphysema and bullae.
3. Special type pneumothorax
(1) Menstrual pneumothorax: Recurrent pneumothorax related to menstrual cycle. This disease was first reported by Maurer in 1958, and was officially named as menstrual pneumothorax by Lillington in 1972. Its incidence rate is only 0.9% of female spontaneous pneumothorax, accounting for about 5.6% of female pneumothorax patients under 50 years old.
The cause of this disease is mainly related to endometriosis of lung, pleura or diaphragm. The exact pathogenesis is not clear, but some theories have been put forward to explain the pathogenesis of this disease:
① Endometriosis in thoracic cavity: The reason is that pneumothorax attack is closely related to menstrual cycle; Many cases found endometriosis in the chest cavity; This disease is more common on the right side, which is consistent with the position of endometriosis in the chest. The onset age of both cases is the same. Because of endometriosis in the chest, endometriotic lesions in bronchioles are congested and swollen during menstruation, which makes the lumen partially blocked, forming a "valve" effect, which leads to the rupture of pleura due to local expansion at the distal end, but there are also unexplained phenomena: about 75% of cases undergoing thoracotomy for this disease have not found endometriotic lesions; Patients with thoracic endometriosis are often accompanied by pleural effusion and menstrual hemoptysis, while menstrual pneumothorax is not accompanied by hemoptysis and pleural effusion, so menstrual pneumothorax caused by endometriosis only represents the cause of partial pneumothorax.
② Diaphragmatic pore theory: According to the embryonic development and anatomical physiology of diaphragm, the ways of gas entering the chest from abdominal cavity are: congenital defects of diaphragm, such as Morgagni pore and Bochdalek pore; Laceration of normal esophagus, aorta and inferior vena cava on diaphragm; Congenital diaphragmatic rupture, such as hiatus after diaphragm ectopia, pneumothorax after pneumoperitoneum treatment in pulmonary tuberculosis patients, has proved that there is a pathway between chest and abdomen, but there is no spontaneous pneumothorax caused by diaphragm defect in men. 1 case of spontaneous pneumothorax complicated with pneumoperitoneum has been found abroad. Radionuclide imaging has been tried to prove that the chest and abdomen are connected, but the results are not supported. The above data further confirmed the specific pathogenesis of women. During menstruation, the uterine contraction is uneven, which may make air enter the uterine cavity and reach the abdominal cavity through the fallopian tube, which coincides with the shedding of ectopic endometrial tissue blocking the diaphragm hole, the diaphragm channel is temporarily opened, and the gas is sucked into the pleural cavity from the diaphragm hole under the action of the negative pressure suction pump. During non-menstrual period, mucus emboli seal the cervix and block gas from entering the chest from the reproductive tract. This theory can explain many clinical signs of this disease, such as pneumothorax caused by diagnostic artificial pneumoperitoneum; Pneumothorax can be cured after tubal ligation or hysterectomy. However, endometriosis and diaphragmatic defect are rare, accounting for only 65,438+09%, and many cases still recur after operation to block the diaphragmatic channel. So we can't use this theory alone to make a comprehensive and reasonable explanation.
(3) (3) Kovarik and other theories: It is believed that the endometrial tissue in the pelvic cavity may spread to the subpleural lung through diaphragm defect or blood flow and lymph to form lesions, and fall off during menstrual period, leading to lung leakage and pneumothorax. Japanese scholars reported 1 case that the diaphragm was normal after thoracotomy, but endometrial tissue was found around the ruptured pulmonary bulla, which further supported this theory.
④ The increase of prostaglandin (mainly prostaglandin F2a) is related to menstrual pneumothorax: prostaglandin F2a can regulate the contraction function of pulmonary blood vessels and bronchial smooth muscle. Rossi believes that this disease is caused by the increase of prostaglandin F2a in blood during menstruation, which makes bronchial smooth muscle contract and the pressure in airway increase, leading to the rupture of alveoli and pleura and pneumothorax. Prostaglandin F2a can cause endometrial necrosis, but there is still insufficient evidence.
(2) Pregnancy complicated with pneumothorax: most of them are young women in reproductive period. Patients with this disease will have pneumothorax every time they get pregnant. According to the time of pneumothorax, it can be divided into early (3-5 months of pregnancy) and late (more than 8 months of pregnancy). The mechanism of its occurrence is not very clear. Some people think it is related to the changes of adrenocortical hormone level and thoracic compliance. Some scholars think that pneumothorax in early pregnancy is related to the decrease of adrenocortical hormone level (it is reported in the literature that the urine content of patients is 3.25 μ mol/24h (1.18mg/24h) at ordinary times, but it drops to 2.125 μ mol/24h (0.77mg/24h) during pregnancy, but others think it is pregnancy.
(3) Spontaneous pneumothorax in the elderly: Spontaneous pneumothorax in people over 60 years old is called spontaneous pneumothorax in the elderly. In recent years, the incidence of this disease has increased, with more males than females, and most of them are secondary to chronic lung disease (about 90%), among which chronic obstructive pulmonary disease is the first, and its pathogenesis is not very clear, but it may be that on the basis of the original chronic lung disease, the alveolar elasticity and systemic resistance are reduced due to the aging of the whole body tissues and organs of the elderly.
(2) Pathogenesis
With the development of science and technology, especially the further improvement and progress of optical technology, micro-camera system and high-definition imaging system, VATS (Video Assisted Thoracoscopy) has been widely used in clinic. Because video-assisted thoracoscope can thoroughly and carefully examine the whole lung surface lesions, and can magnify and observe the subtle lung pleural lesions under high-definition endoscope and TV display, Vanderscheren clinically divides spontaneous pneumothorax into four grades according to the adhesion degree between alveolar lesions and pleura under video-assisted thoracoscope: Grade I is idiopathic pneumothorax. Grade ⅱ is pneumothorax with adhesion of visceral layer and parietal pleura; Grade ⅲ is visceral subpleural vesicle, with a diameter of 2cm. This classification method has clinical practical value in guiding the selection of reasonable treatment methods, such as grade ⅰ idiopathic pneumothorax, which is almost normal by direct observation with naked eyes. However, when magnified by the newly emerging high-definition endoscope and TV monitor, pulmonary bullae with a diameter of 1 ~ 2 mm can be found, which can be directly coagulated and sealed by laser or electrotome through endoscope, or induced by talcum powder. , can still be directly solidified by laser or electrotome, and the fibrin is Grade II. 2cm pulmonary bullae, but different pleurodesis methods must be added. Grade ⅳ is multiple giant pulmonary bullae. Those who can tolerate thoracotomy can simply perform bullectomy or wedge resection. Those who can't tolerate thoracotomy can be injected with talcum powder (or tetracycline hydrochloride, etc. Thoracoscopic pleurodesis was performed.
According to the patients with pulmonary bullae or spontaneous pneumothorax who underwent thoracotomy and histological examination, some scholars divided pulmonary bullae into three types: type I: thin-walled cyst, almost unconnected with bronchus, basically outside the lung, single cavity, no trabecular bone in the cavity, several centimeters in diameter, sometimes up to 15 ~ 25 cm, which is obvious on common chest radiographs, forming tension bullous emphysema. For this type, type ⅱ: pulmonary bullae with medium diameter and thick fibrotic wall are located in the deep part of lung parenchyma and belong to pulmonary bullae. The vesicles are separated by many spaces. Only the superficial part was seen under thoracoscope, and several type ⅱ pulmonary bullae were seen in one lung. The patient may be asymptomatic, but the X-ray chest film may not show it, but the rupture of pulmonary bullae will cause spontaneous pneumothorax. Generally, the ruptured pulmonary bullae can be seen under thoracoscope. Type ⅲ: bulla. There are many trabeculae in pulmonary bullae, which are widely connected with bronchi. This type is the most common cause of diffuse bullous emphysema. Once ruptured, spontaneous pneumothorax will be formed, with high morbidity and mortality.
Ohata et al. reported in 1980 that 253 cases of 334 patients with spontaneous pneumothorax underwent thoracotomy, among which 126 cases underwent histological optical microscopy. According to the observation of scanning electron microscope, 60 cases of emphysema bullae were divided into three types: Reid type ⅰ, Reid type ⅱ and giant bullae. Reid type is characterized by excessive expansion of lung tissue to form pulmonary bullae, narrow neck and clear boundary with the whole lung structure. Pleura in the bulla becomes thinner, mesothelial cells on the surface are sparsely distributed, and some areas are even completely missing, so that collagen fibers are exposed and pores or cracks of several microns can be seen. The basal wall of the bulla is flat, composed of amorphous substances and scattered with oval holes. During the operation, it was observed through a microscope that air leakage was caused by air holes. Electron microscopic examination showed that mesothelial cells were completely lacking around pores, and there was no cellular material on the inner surface of bullae, which was replaced by wavy collagen fiber bundles, Reid. The neck is wide and the boundary with the whole lung tissue is unclear. Electron microscopic examination showed that mesothelial cells on the pleural surface of bullae were relatively complete, with short microvilli, but there were still areas covered by mesothelial cells, like Reidⅰⅰ type bullae, and the degenerated alveoli were exposed in the cavity of bullae. Alveolar structure is relatively normal, and Cohen's pore can be seen. Giant pulmonary bullae are larger, accounting for more than 65,438+0/3 of the unilateral thoracic cavity. The wall of bulla is thin and translucent. Under electron microscope, the surface of bulla is almost normal, with mesothelial cells of normal size, short microvilli and normal alveolar structure. Therefore, according to the pathology of pneumothorax, the author further expounds its pathogenesis and thinks that the formation of spontaneous pneumothorax is not necessarily based on the rupture of pulmonary bullae. But it may also be due to the scarcity or complete lack of pleural mesothelial cells (such as Reidⅰⅰ type). With the increase of lung pressure, air enters the pleural cavity through the holes in the wall of pulmonary bullae, which emphasizes that pleural mesothelial cells play an important role in the occurrence of spontaneous pneumothorax.