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what are the causes of pneumothorax and pneumothorax

what are the causes of pneumothorax and pneumothorax

Etiology of pneumothorax

(a) the cause of the disease

According to the presence or absence of primary diseases, spontaneous pneumothorax can be divided into two types: primary pneumothorax and secondary pneumothorax.

The factors inducing pneumothorax are strenuous exercise, cough, lifting heavy objects or upper arm high, weightlifting, defecation and so on. When coughing violently or defecating forcibly, the pressure in alveoli increases, causing the original damaged or defective lung tissue to rupture and cause pneumothorax. Using artificial respirator, if the air supply pressure is too high, pneumothorax may occur. According to statistics, 50% ~ 60% of cases can't find obvious inducement, and about 6% of patients even get sick in bed rest.

1. Primary pneumothorax is also called idiopathic pneumothorax. It refers to the pneumothorax of healthy people whose lung routine X-ray examination fails to find obvious pathological changes, which is easy to occur in young people, especially male thin elders. According to foreign literature reports, this kind of pneumothorax accounts for the first place of spontaneous pneumothorax, while secondary pneumothorax is the main one in China.

The cause and pathological mechanism of this disease are not very clear. Most scholars believe that it is caused by the rupture of subpleural microvesicles (bleb) and pulmonary bullae (bulla). According to the histopathological examination of pulmonary bullae in patients with idiopathic pneumothorax, It is based on subpleural nonspecific inflammatory scar, that is, nonspecific inflammation around bronchioles causes hyperplasia of elastic fibers and collagen fibers in visceral pleura and subpleura to form scar, which can reduce the elasticity of adjacent alveolar wall, lead to alveolar rupture and form pulmonary bullae under pleura. Non-specific inflammation of bronchioles itself plays the role of one-way valve, which makes emphysematous changes in interstitium or alveoli and forms pulmonary bullae.

Some scholars believe that congenital hypoplasia of lung tissue is the cause of pulmonary bullae. That is, due to congenital dysplasia of elastic fibers, and low elasticity, the alveolar wall expands to form bullae and rupture. Marfan syndrome (a congenital inherited connective tissue deficiency) is a typical example of spontaneous pneumothorax. There are reports of familial spontaneous pneumothorax abroad, 11 of 725 cases of spontaneous pneumothorax reported by Miyagi have family history, and Kimura reported that spontaneous pneumothorax occurred at the same time, which may mean the existence of genetic factors.

Among the causes of this disease, some people put forward "neomembrane theory", collateral ventilation disorder mechanism, air pollution theory and so on.

2. The mechanism of secondary pneumothorax is the formation of pulmonary bullae or direct injury to pleura on the basis of other lung diseases. On the basis of chronic obstructive emphysema or post-inflammatory fibrotic lesions (such as silicosis, chronic pulmonary tuberculosis, diffuse pulmonary interstitial fibrosis, cystic pulmonary fibrosis, etc.), bronchiolitis is narrow and distorted, resulting in valve mechanism and pulmonary bullae. The swollen emphysema vesicles are degenerative due to nutritional and circulatory disorders. When coughing, sneezing or increasing pulmonary pressure, it leads to rupture of pulmonary bullae and pneumothorax. Among the 179 cases of spontaneous pneumothorax reported by Wu et al., chronic bronchitis complicated with emphysema accounted for the first place (38.5%), followed by pulmonary tuberculosis (17.3%), idiopathic pneumothorax (13.4%), Staphylococcal pneumonia (12.3%), and the rest were caused by other reasons.

Staphylococcus aureus, anaerobic bacteria or gram-negative bacilli caused by suppurative pneumonia, lung abscess lesions rupture to the chest, resulting in pus pneumothorax. Fungi or parasites and other microorganisms infect pleura and lung, infiltrate or penetrate visceral pleura and cause pneumothorax. Rupture of bronchopulmonary cyst can be complicated with pneumothorax. In addition, perforation of adjacent organs such as esophagus into pleural cavity, application of positive pressure artificial ventilation and long-term use of glucocorticoid can also cause pneumothorax.

In recent years, secondary pneumothorax caused by some diseases has been paid more and more attention: ① With the development of comprehensive treatment, the survival time of lung cancer patients is gradually prolonged, and pneumothorax secondary to lung cancer will increase day by day; Its incidence rate accounts for 4% of lung cancer patients (especially in advanced small cell lung cancer). The causes are: tumor blocks bronchioles, resulting in localized emphysema; Obstructive pneumonia further develops into pulmonary suppuration, and finally breaks to the chest cavity; The tumor itself invades or destroys the visceral pleura. ② Sarcoidosis, mainly the third stage, and the incidence of pneumothorax was 2% ~ 4%. It is caused by the formation of subpleural bullae caused by late fibrosis or the direct invasion of pleura by granulomatous lesions. ③ Histiocytosis X: It is reported that the incidence of spontaneous pneumothorax can reach 20% ~ 43%, which is related to the obvious pulmonary fibrosis in the late stage of the disease, which finally leads to "honeycomb lung" and the formation of pulmonary bullae. ④ Pulmonary lymphangioleiomyomatosis (LAM): According to literature reports, about 40% of patients are complicated with spontaneous pneumothorax. Taylor reported that of 32 cases of LAM, 26 (81%) developed pneumothorax. The occurrence of this disease is closely related to the changes of estrogen in vivo. Parabronchial smooth muscle hyperplasia can partially or completely block the airway, causing pulmonary bullae and cyst, and finally leading to rupture and pneumothorax. AIDS: The incidence of spontaneous pneumothorax is 2% ~ 5%. Coker et al. reported that the incidence of pneumothorax in 298 AIDS cases was 4%. Its mechanism may be as follows: the disease is easy to invade pleural and lung tissue, and it is easy to develop pneumocystis carinii pneumonia, which has destructive effect on lung and pleura and leads to pneumothorax; The direct cytotoxic effect of human immunodeficiency virus (HIV) on lung macrophages causes the release of elastase, which leads to emphysema and the formation of pulmonary bullae.

3. Special types of pneumothorax

(1) Menstrual pneumothorax: Repeated pneumothorax related to menstrual cycle. This disease was first reported by Maurer in 1958 and officially named menstrual pneumothorax by Lillington in 1972. Its incidence rate is only 0.9% of female spontaneous pneumothorax, and about 5.6% of female pneumothorax patients under 50 years old.

The causes of endometriosis are mainly related to endometriosis of lung, pleura or diaphragm. The exact pathogenesis is still unknown. However, some theories have been put forward to try to explain the pathogenesis of this diseaseSystem: ① Intrathoracic endometriosis theory: the reason is that pneumothorax attack is closely related to menstrual cycle; Many cases found endometriosis in thoracic cavity; The right side of this disease is more common and consistent with the position of endometriosis in thoracic cavity; The age of onset is the same in both. Due to the existence of endometriosis in the thoracic cavity, the endometrial lesions in bronchioles are congested and swollen during menstruation, which makes the lumen partially blocked and forms a "valve" function, resulting in local hyperinflation at the distal end and pleural rupture. However, there are also unexplained phenomena: about 75% of the cases of thoracotomy due to this disease have not found endometriosis lesions; Patients with thoracic endometriosis often have pleural effusion and menstrual hemoptysis, while menstrual pneumothorax is not accompanied by hemoptysis and pleural effusion, so menstrual pneumothorax caused by endometriosis only represents part of the etiology of pneumothorax. ② Diaphragm channel hiatus theory: From the embryonic development and anatomical physiology of diaphragm, the ways of gas entering thoracic cavity from abdominal cavity are: congenital defects of diaphragm, such as Morgagni hole and Bochdalek hole; Normal hiatus of esophagus, aorta and inferior vena cava on diaphragm; Congenital rupture of diaphragm. Such as diaphragm ectopic endometrial shedding after the formation of a hole, Meigs' syndrome and pulmonary tuberculosis patients with pneumothorax after pneumoperitoneum treatment has been confirmed the existence of thoracoabdominal pathway. However, there is no spontaneous pneumothorax caused by septal muscle defect in men. A case of spontaneous pneumothorax with pneumoperitoneum was found abroad, and it was tried to prove that there was communication between chest and abdomen by radionuclide imaging, but the results did not support it. The above data further confirm the female-specific pathogenesis. During menstruation, due to uneven uterine contraction, air may enter the uterine cavity and reach the abdominal cavity through fallopian tubes. At this time, the ectopic endometrial tissue that occluded the diaphragm orifice fell off, the diaphragm channel was temporarily opened, and the gas was sucked into the pleural cavity from the diaphragm hiatus under the action of the thoracic negative pressure suction pump. Instead of menstrual period, mucus emboli seal the cervix and block gas from the reproductive tract into the chest cavity. This theory can explain many clinical signs of this disease, such as making diagnostic artificial pneumoperitoneum can induce pneumothorax; Pneumothorax can be cured after tubal ligation or hysterectomy. However, diaphragm endometriosis and defect are rare, accounting for only 19%, and many cases still recur after blocking diaphragm channel by surgery, so this theory can not be used for a comprehensive and reasonable explanation. ③ Kovarik and other theories: It is believed that the endometrial tissue in pelvic cavity may spread to the lung subpleura through diaphragm defect or blood flow and lymphatic pathway to form lesions, and fall off during menstruation, resulting in gas leakage in the lung and pneumothorax. Japanese scholars reported that a case of diaphragm abnormality was not found through thoracotomy, but endometrial tissue was found around ruptured pulmonary bullae, which further supported this theory. The elevated level of prostaglandin (mainly prostaglandin F2a) is related to menstrual pneumothorax: prostaglandin can regulate the diastolic and contractile functions of pulmonary vessels and bronchial smooth muscle. Rossi believes that this disease is caused by the increase of prostaglandin F2a level in blood during menstruation, which makes bronchial smooth muscle contract, increases airway pressure, and promotes alveolar and pleural rupture to form pneumothorax. And prostaglandin F2a can cause endometrial necrosis. However, there is still a lack of sufficient evidence.

(2) Pregnancy complicated with pneumothorax: Most of them are young women in reproductive period. Pneumothorax occurs in patients with this disease due to every pregnancy. According to the time of pneumothorax, it can be divided into early stage (3 ~ 5 months of pregnancy) and late stage (more than 8 months of pregnancy). Its mechanism is not very clear. Some people think that it is related to the change of adrenocortical hormone level and thoracic compliance. Some scholars think that pneumothorax in early pregnancy is related to the decrease of adrenocortical hormone level (literature reports that the urine 17-hydroxysteroid content of patients is 3.25 μ mol/24h (1.18 mg/24h) at ordinary times, but it drops to 2.125 μ mol/24h (0.77 mg/24h) during pregnancy. However, it is also believed that adrenal cortex hyperfunction during pregnancy inhibits the repair of connective tissue injury. Spontaneous pneumothorax in late pregnancy may be related to the increase of intrathoracic pressure caused by low thoracic compliance.

(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 an increasing trend. There are more men than women. Most of them are secondary to chronic pulmonary diseases (about 90%), among which chronic obstructive pulmonary diseases occupy the first place. The mechanism is not very clear, but it may be based on the original chronic lung diseases, due to the aging of the whole body tissues and organs of the elderly, the alveolar elasticity decreases, and the whole body resistance decreases, which can cause alveolar rupture and pneumothorax in general activities, even coughing, sneezing, holding breath and defecating.

(B) 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. Thoracoscopy can thoroughly and carefully examine the whole pulmonary surface lesions, and can be magnified to observe subtle pulmonary pleural lesions under high-definition endoscopy and television display. Vanderscheren divided spontaneous pneumothorax into four grades clinically according to the adhesion between alveolar lesions and pleura under thoracoscope: Grade I was idiopathic pneumothorax, and there was no obvious abnormality in lung tissue observed under endoscope; Grade ⅱ is pneumothorax with visceral and parietal pleural adhesion; The third grade is the visceral subpleural vesicle and its diameter<2cm的肺大疱;Ⅳ级有多个直径>2cm pulmonary bullae, this grading method has clinical practical value for guiding the selection of reasonable treatment methods. For example, grade I idiopathic pneumothorax has a nearly normal appearance under direct naked eye observation. However, lung blisters with a diameter of 1 ~ 2mm can be found by magnifying observation under the newly appeared high-definition endoscope and TV display, which can be directly coagulated and sealed by laser or electrotome through endoscope, or induced by talcum powder for pleural fixation. Class II can still be coagulated directly by laser or electrotome, or sealed with fibrin glue, but the adhesion band must be decomposed during operation. Lung bullae with diameter less than 2cm can be coagulated directly by laser in grade ⅲ, but pleural fixation in different ways must be added. Grade IV is multiple giant pulmonary bullae, which can bearFor thoracotomy, simple bullous resection or wedge resection of lung can be performed. Those who can't tolerate thoracotomy will be sprayed with talcum powder (or tetracycline hydrochloride, etc.) for pleural fixation through video-assisted thoracoscope.

Some scholars divide pulmonary bullae into three types according to thoracotomy and histological examination of patients with pulmonary bullae or spontaneous pneumothorax: type I: thin-walled cyst, which is almost disconnected from bronchus, basically belongs to extrapulmonary nature, single cavity, no trabecula in cavity, and its diameter is generally several centimeters, sometimes up to 15 ~ 25cm, which is obvious on ordinary X-ray chest film. And form tension bullous emphysema. Surgical resection of bullae for this type has the best therapeutic effect. Type II: Bullae is medium diameter, fibrotic thick-walled, located in the deep part of lung parenchyma, belonging to pulmonary bullae. The bullae is separated by many intervals. Only the surface part can be seen under video-assisted thoracoscope. Several type ⅱ pulmonary bullae can be seen in one lobe of lung. Patients may be asymptomatic. X-ray chest film can also have no performance. However, spontaneous pneumothorax is caused when bullae rupture. Ruptured bullae can usually be seen under video-assisted thoracoscope. Type III is a large bullae, which exists in not only one lung lobe, with multiple trabeculae and extensive communication with bronchus. This type is the most common cause of diffuse bullous emphysema. Once ruptured, it will form spontaneous pneumothorax, and its morbidity and mortality are high.

In 1980, Ohata reported that 253 of 334 patients with spontaneous pneumothorax underwent thoracotomy, and 126 of them underwent histological optical microscopy. On the basis of scanning electron microscopy, 60 cases of emphysematous bullae were divided into three types: Reid ⅰ, Reid ⅱ and giant bullae. Reid ⅰ is characterized by excessive expansion of lung tissue to form bullae, narrow neck and clear boundary with the whole lung structure; The pleura in the bullae is thinned, the mesothelial cells on the surface are sparse, and even completely lacking in some areas, so that collagen fibers are exposed, and small holes or fissures with the size of several microns can be seen. The basal wall of bullae is flat and composed of amorphous substances, with scattered oval pores. During the operation, air leakage caused by small holes was observed by microscope, and mesothelial cells were completely absent around the small holes by electron microscope. There is no cellular material on the inner surface of bullae, but it is replaced by wavy collagen fiber bundles. Reid ⅱ type is characterized by shallow pulmonary bullae; The neck is wide and the boundary between it and the whole lung tissue is unclear. Electron microscopic examination showed that the mesothelial cells on the pleural surface of bullae were relatively complete and short microvilli were seen. However, there are still areas without mesothelial cell coverage, and like Reid I bullae, the deteriorated alveoli are exposed to the cavity of bullae; The alveolar structure is relatively normal, and Cohn hole can be seen. Huge bullae is large in volume, occupying more than 1/3 of unilateral thoracic cavity, and its wall becomes thin and translucent. Electron microscopy showed that the surface of bullae was almost normal, with normal size mesothelial cells, thick and short microvilli and normal alveolar structure. Therefore, according to the pathology of pneumothorax, the author further clarified its pathogenesis, It is considered that the formation of spontaneous pneumothorax is not necessarily based on the rupture of bullae, but may be caused by the scarcity or complete lack of pleural mesothelial cells (such as Reid ⅰ type). Under the condition of increased pulmonary pressure, air enters the pleural cavity through the hiatus of bullae wall, and it is emphasized that pleural mesothelial cells play an important role in the occurrence of spontaneous pneumothorax.

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