Obstructive emphysema
Introduction
Introduction to obstructive emphysema Obstructive pulmonary emphysema (obstructive pulmonary emphysema) refers to the persistent expansion and enlargement of the distal balloon lumen of the terminal bronchioles (including respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli), accompanied by structural damage of the air wall without significant fibers. A disease that becomes a pathological feature. Chronic bronchitis is induced by long-term smoking, air pollution, inhalation of harmful chemicals and dust, and chronic recurrent respiratory infections, further developing the disease. basic knowledge The proportion of sickness: 0.6%-4.3% Susceptible people: smokers, mine workers Mode of infection: non-infectious Complications: obstructive emphysema, respiratory failure, chronic pulmonary heart disease, gastric ulcer
Cause
Causes of obstructive emphysema
(1) Causes of the disease
The etiology of obstructive emphysema is extremely complex and is briefly described below.
Smoking
Cigarettes contain a variety of harmful ingredients such as tar, nicotine and carbon monoxide. Smokers have increased fucoidan and neuraminic content in mucous glands, which can inhibit bronchial mucociliary activity, reflexive bronchospasm, and weaken alveolar phagocytes. Smokers who have emphysema or chronic bronchitis and die from respiratory failure or pulmonary heart disease are far more likely than non-smokers.
2. Air pollution
Autopsy materials have shown that under similar climate and economic conditions, the incidence of emphysema in areas with severe air pollution is higher than in less polluted areas.
3. Infection
Respiratory viruses and bacterial infections are associated with the development of emphysema. Repeated infection can cause bronchial mucosa congestion, edema, glandular hyperplasia, hypertrophy, hypersecretion, thickening and narrowing of the wall, causing airway obstruction. Increased protease activity in pulmonary infection may also be associated with emphysema formation.
4. Protease-antiprotease balance imbalance
Some proteolytic enzymes in the body have a digestive effect on lung tissue, while anti-protease has an inhibitory effect on various proteases such as elastase. The balance between protease and anti-protease is an important factor in maintaining the normal structure of lung tissue from damage. There are two sources of proteases for digesting lung tissue, exogenously derived from pathogens such as bacteria and molds, endogenously derived from neutrophils and alveolar macrophages. Smoking increases elastase activity and inactivates anti-protease.
1 antitrypsin is a glycoprotein synthesized by the liver that inhibits the activity of various serine proteases. Alpha 1 antitrypsin is controlled by a pair of autosomal recessive genes, which are normal humans because of the M type, ie PiMM. If glutamic acid is replaced by lysine, it is Z-form. In the foreign data report population, PiZZ homozygotes accounted for about 1/4000, and PiMZ heterozygotes accounted for about 3% to 5%. PiZZ homozygotes have a severe decrease in 1 antitrypsin activity in their serum. Susceptible to hepatitis and emphysema. The emphysema caused by 1 anti-trypsin deficiency has the following characteristics: early onset age, no smoking history; shorter course, more acute urgency; serum protein electrophoresis showed decreased 1 globulin and decreased serum 1 antitrypsin activity. Pathologically, it is mostly lobular emphysema. The incidence of emphysema in other types such as PiSS and various heterozygotes PiMZ and PiSZ is not increased. Alpha 1 antitrypsin deficiency is more common in Caucasians and is rare in China.
(two) pathogenesis
Chronic bronchial inflammatory injury
Various factors causing chronic bronchitis such as infection, smoking, air pollution, long-term inhalation of occupational dust and harmful gases, and allergic factors can cause chronic inflammation of the bronchial tubes, causing incomplete occlusion of the lumen, resulting in inhalation. Gas easily enters the alveoli, and when exhaled, due to increased pressure in the pleural cavity, the bronchus is further closed, resulting in excessive residual gas in the alveoli and hyperinflation of the alveoli. Chronic inflammation can also damage the cartilage tissue of the small bronchus wall, causing the bronchi to lose its normal scaffold. And exhaled, the bronchus is easy to trap, hindering the discharge of gas, causing excessive accumulation of air in the alveoli, increased pressure and excessive expansion of the alveoli, and, in addition, due to the increase of the alveolar pressure, the capillaries of the alveolar wall are compressed, the lungs Tissue blood supply reduction and nutritional disorders can also cause alveolar wall elasticity to decline. Therefore, chronic bronchial inflammatory injury is an important cause of obstructive emphysema.
The mechanism of COPD airway inflammation is that when the body is stimulated by factors such as smoking, infection and environmental pollution, monocytes, macrophages and neutrophils rapidly synthesize and release cytokines such as IL-1 and TNF-. , IFN, etc., these factors can induce the increase of vascular endothelial cell synthesis adhesion molecules (ICAM-1, VCAM-1), in addition, can also activate adhesion molecules on the surface of leukocytes (LFA-1, VLA-4, MAC-1, etc.) It up-regulates its expression and interacts with the corresponding adhesion molecules on endothelial cells, leading to rapid adhesion of leukocytes, and translocation to the inflammatory site across the endothelium to participate in the inflammatory response, while the above-mentioned pathogenic factors such as smoking, infection and other damage to the lung tissue It can also stimulate epithelial cells. Macrophages produce neutrophil chemokine IL-8, macrophage inflammatory protein-2 (MIP-2), activate and chemotaxis of neutrophils at target sites, which aggravates Inflammatory response, in addition, activated neutrophils release proteolytic enzymes and elastase can cause bronchial epithelial shedding, ciliary movement is reduced, mucus secretion is hyperthyroidism, leading to mucus retention and bacterial reproduction, making inflammation Recurrence and prolonged unhealed.
2. Protease-antiprotease balance imbalance
At present, some proteolytic enzymes in the body have the effect of damage and damage to lung tissue, while anti-protease has inhibitory effect on various proteases such as elastase. Protease and anti-protease maintain balance are important to ensure the normal structure of lung tissue from damage. Factors such as anti-protease deficiency or increased protease can lead to emphysema in the destruction of lung tissue structure.
(1) Anti-protease: an anti-protease system in human body, that is, a protease inhibitor, wherein 1-antitrypsin (1-AT) is the most active one, in addition, 2- Macroglobulin (2-M) and antileukoprotease (ALP), 1-AT is an acute phase reaction protein synthesized by the liver with a molecular weight of 45-56 KD and a normal serum concentration of 1360±176 mg/L. In a variety of inflammatory reactions, serum 1-AT levels can be increased, which can inhibit the activity of various serine proteases. 2-M is mainly synthesized by hepatocytes, and has a large molecular weight. When vascular permeability increases, the level of lung tissue begins. Elevated, ALP synthesis and excretion are in the airway, and have the effect of inactivating elastase. Therefore, under normal conditions, 1-AT, 2-M and ALP synergistically protect the lungs and airways from proteases. damage.
(2) Protease: The main source of proteases that destroy lung tissue is two: an exogenous protease from pathogenic bacteria; two endogenous proteases from neutrophils and macrophages, in which human neutral elastase (HNE) The most important, and the most serious pathogenesis of emphysema, HNE is a serine protease, each containing about 3mg of neutrophils, 106 granulocytes can hydrolyze 0.4mg of lung elastin in vitro, 1-AT can It is 1:1 combined with HNE to form a complex that is not easily dissociated, and the elastase is inactivated. Macrophage elastase is a metalloproteinase. It needs to have a metal ion to function, and the protease content in macrophages. It is only equivalent to 1/10 of neutrophils, which is not inhibited by 1-AT, but instead can hydrolyze 1-AT and lose its anti-HNE effect.
When bronchial-pulmonary infection or long-term stimulation of cigarette smoke and other harmful substances, alveolar macrophages and neutrophils aggregate and activate, releasing elastase, when the content and activity of protease exceeds the resistance in local lung tissue. When the protease (1-AT-based) inhibits the potency, the elastin is degraded, causing the lung tissue to ablate, the alveolar septum is destroyed, the alveolar cavity is enlarged, and the small airway loses the support of the surrounding space during exhalation and traps, resulting in trapping. The occurrence of emphysema.
In addition, during the development of emphysema, neutrophils and alveolar macrophages also generate and release oxygen free radicals, which oxidize the active core methionine in 1-AT to form sulfoxide, thereby making it resistant to proteases. Significantly, smokers' 1-AT activity is only 60% of non-smokers. Therefore, smoking can disrupt the balance of protease-anti-protease system and promote the occurrence and development of emphysema.
3. Genetic factors
The occurrence of emphysema is also related to genetic factors. In normal human serum, 1-AT is inherited by autosomal recessive genes. In the genetic process, the majority of normal populations are composed of two M-type alleles. The zygote, the genetic phenotype is PiMM, the carrier's 1-AT serum concentration is normal (>250mg/dl), the homozygote consists of two Z-type alleles, PiZZ is its phenotype, and its serum 1-AT is only 10% to 15% (<50mg/dl) of normal people, the number of people carrying the genetic phenotype is very small, only about 1:2000 (0.05%-0.07%) in the Caucasian population; in addition, related to 1-AT deficiency Heterozygous, whose genetic phenotype is PiSS, is heterozygous for the combination of two different alleles, with more genetic phenotypes (4% to 4.7%), followed by PiMS (0.5%) and PiSZ ( 0.08% to 0.14%), the remaining heterozygous phenotypes are more common. According to a survey of 3,724 Chinese people, the 1-AT genetic phenotype is still mainly PiMM, and one PiZZ homozygote is not found. Other types such as PiSS and PiMZ The incidence of emphysema such as PiSZ is not high. Therefore, emphysema caused by hereditary 1-AT deficiency is not important in China.
4. Pathological changes
Gross examination showed excessive expansion of the lungs, decreased elasticity, and the lungs could not be retracted after thoracotomy. The appearance was gray or pale. There were many large bubbles of different sizes on the surface. Under the microscope, the balloon swell at the distal end of the terminal bronchioles was narrowed. The elastic fibers become thin or broken, the alveolar wall becomes thinner, the alveolar pores expand, the alveolar ruptures or forms a large bubble, the small blood vessels associated with the bronchioles show inflammatory changes, the smooth muscle of the media is smooth, the degeneration and necrosis, the lumen is narrow or even Occlusion, due to erosion of alveolar rupture and inflammation, the number of pulmonary capillary beds and the cross-sectional area were reduced. The pathological changes of bronchioles in emphysema were the same as those of chronic bronchitis.
According to the location of emphysema involving the lobules of the lungs, obstructive emphysema can be divided into the following three types:
(1) Central lobe emphysema: more common in the upper part of the lung, due to inflammation of the terminal bronchioles or primary respiratory bronchioles due to inflammation, the distal secondary respiratory bronchioles cystic dilatation It is characterized by a cystic dilated respiratory bronchiole located in the central region of the secondary leaflet (Figure 3).
(2) Total lobular emphysema: diffusely invaded the whole lung, but the former lower part is more common, due to the respiratory bronchial stenosis caused by the terminal lung tissue, namely the alveolar duct-alveolar sac and alveolar expansion, It is characterized by a small cystic cavity that is spread throughout the lobules of the lung (Figure 4).
(3) Mixed emphysema: There are pathological changes of the above two types in the same lung, mostly on the basis of the central type of the lobule, and the lung tissue in the peripheral area of the lobular swell is expanded.
Prevention
Obstructive emphysema prevention
Focus on preventing the development of patients with chronic bronchitis as airflow limitation, including promoting smoking is harmful to health, smokers should immediately quit smoking; avoid harmful dust, smoke or gas inhalation, factories, mines should be treated with dust and harmful gases, such as Wet operation, closed dust source, enhanced ventilation and personal protection; prevention of respiratory infections, including viruses, mycoplasma or bacterial infections, regular injection of influenza vaccine, pneumococcal vaccine, etc. have a certain significance for the prevention of susceptible; for patients with chronic bronchitis Regular monitoring of pulmonary ventilation function (FEVl, FEVl/FVC and FEVl%), early detection of airflow limitation, and appropriate prevention measures; in addition, improve patient living standards, increase nutrition, strengthen health education, improve working environment And conditions, to develop good health habits, etc., have important significance for the prevention and treatment of this disease, in addition to avoid cold and emotional stimulation, avoid tobacco and fat diet and contact with irritating gases, red dates, Chinese yam, lily, Walnut kernels are eaten.
Complication
Obstructive emphysema complications Complications obstructive emphysema respiratory failure chronic pulmonary heart disease gastric ulcer
Symptom
Symptoms of obstructive emphysema Common symptoms Barrel chest and chest tightness dyspnea dyspnea breath sounds weakened, urgency, chest tightness, suffocation, exhalation, cheeks, bulging, lip snoring, prolonged labor, shortness of breath, difficulty breathing
symptom
The disease is insidious, with chronic bronchitis as the cause, and has a history of cough and cough for many years. Smokers often cough and cough mucus after getting up in the morning, and when they have respiratory infections, they have mucopurus, cough, and cough. Symptoms are more severe in winter, and gradually reduce when the climate warms up in the next year. Coughing is severe in patients with severe disease, coughing is present for a long time, and there is no regularity of seasonal changes in winter and summer. Patients with emphysema often have symptoms of air urgency. If you go to the building or walk quickly, you will feel anxious. If you are going to go to Pingping Road, you will feel anxious. If you are talking, dressing, washing your face or even resting, there is an air urgency, suggesting that the emphysema is quite serious, and there is still fatigue and anorexia. Systemic symptoms such as weight loss, acute respiratory failure or right heart failure may occur, and headache may indicate CO2 retention in patients with emphysema. Further analysis of arterial blood gas should be performed. Those with hypoxemia may have cyanosis. Secondary erythrocytosis.
There were no abnormalities in the early signs of the disease. The anteroposterior diameter of the thoracic cavity was increased in the patients with severe emphysema. The appearance was barrel-shaped, the intercostal space was full, the thoracic echoes in the percussion increased, the dullness of the heart was reduced or disappeared, the dullness of the liver decreased, and the breath sounds and voices weakened. Exhale, and sometimes the bottom of the lungs can smell dry and wet, and the heart sounds low.
The disease is caused by excessive inflation of the lungs, increased residual air volume, and increased lung transparency by X-ray examination. However, this X-ray sign is not sensitive enough in the early stage, the thorax is full when the emphysema is severe, the ribs are flattened, the intercostal space is widened, and the lateral slices are The anterior and posterior diameter of the thorax increased, the posterior sternal space was too wide, the diaphragm was moved down, the sputum became flat, the transparency of the two lungs increased, the blood vessels in the lung field were slender and sparse, the heart shadow was vertical and narrow, and the thoracic and diaphragmatic activities were visible under fluoroscopy. The degree is weakened, and there is also an increase in lung texture. The increase in transparency of the lung is not obvious, the pulmonary artery in the hilar is widened, and the heart is often enlarged.
Type
The clinical manifestations of obstructive emphysema can be divided into two types, and of course many patients do not meet the typical performance of a certain type.
Bronchitis type (BB type) Emphysema type (PP type) Clinical features Obesity, carbuncles, cyanosis, jugular vein engorgement, lower extremity edema, cough, cough, repeated respiratory infection, edema and right heart failure history weight loss, shortness of breath No sputum, sputum, no lower extremity edema and right heart failure history bronchial mucinal gland hypertrophy significantly not significant emphysema degree is not serious severe ventilation function (FEV1MMEF, MBC, etc.) reduce the slight increase of lung volume, significantly increase the gas distribution Uniform uniform diffusion function normal reduction PaO2 (mmHg) <70 <70 PaCO2(mmHg) >45 >45 Hematocrit>60 >55 Chest X-ray signs emphysema is not significant, lung field is normal or hyperemia, heart enlarges emphysema Significantly, the surrounding pulmonary vessels are slender, the heart is normal or narrow and vertical
[Note] FEV1: forced expiratory volume in the first second
MMEF: Maximum expiratory mid-range traffic
MBC: maximum ventilation
PaO2: Arterial oxygen partial pressure
PaCO2: arterial blood carbon dioxide partial pressure
1, bronchitis type also known as purpura type (BB type) bronchial lesions are heavier, mucosal swelling, mucous gland hyperplasia, emphysema lesions are mild, patients often have years of smoking history and chronic cough, history of cough, physical examination obesity, purpura Jugular vein engorgement, lower extremity edema, both lungs and Luoyin, chest X-ray examination of pulmonary congestion, lung texture thickening, no obvious emphysema sign, pulmonary function test ventilation function is obviously damaged, gas distribution is uneven Functional residual gas and total lung volume increase, diffuse function is normal, arterial oxygen partial pressure is reduced, carbon dioxide partial pressure is increased, hematocrit is increased, and it is easy to develop into respiratory failure and/or right heart failure.
2, emphysema type also known as innocent wheezing type (PP type) emphysema is more serious, but bronchial lesions are not serious, more common in old age, physical weight loss, breathing difficulties, no purpura, patients often take special posture, such as The shoulders are tall, the arms are raised, and the cheeks bulge and contract the lips. The transparency of the lungs of the X-ray chest is increased. Although the ventilation function is also damaged, it is not as serious as the bronchitis type, and the gas distribution is even and residual. The ratio of total lung volume increased, alveolar ventilation was normal and even hyperventilation, so the arterial oxygen partial pressure was not significantly reduced, and the partial pressure of carbon dioxide was normal or decreased.
Examine
Examination of obstructive emphysema
Blood test
Some patients may have erythrocytosis, especially when PaO2 <7.3kPa (55mmHg), white blood cells are more normal, and may increase when combined with respiratory infection.
2. Blood gas analysis
PaO2 is reduced due to dysfunction of ventilation, and PaO2 is decreased. Although the ventilatory load is increased, PaCO2 is still maintained in the normal range through early compensation. When the condition is further developed, CO2 retention may be accompanied by PaCO. 2 rises, causing respiratory acidosis.
3. X-ray inspection
: Thoracic dilatation is full, lung volume is enlarged, rib space is widened, ribs are flat, lateral chest radiograph is widened in anteroposterior diameter, pre-cardiac space is increased, transverse iliac crest is low, iliac flattening, lung field transmittance Increased, sometimes limited localized emphysema or pulmonary blebs with limited transmittance, pulmonary veins in the lung field are slender, sparse, straightening; while the inner texture can be thickened, disordered, and the heart is often vertical The heart shadow is long and narrow, and the thoracic and diaphragmatic movements are weakened under fluoroscopy.
Pulmonary function tests
Emphasis on early measurement, long-term dynamic observation, timely detection, and early diagnosis.
Lung volume was measured as residual gas volume (RV).
Total lung volume (TLC) increased.
The residual air volume/total lung ratio RV/TLC is often >40%.
The ventilatory function measures the increase in airway resistance and the forced expiratory flow rate decreases.
The forced expiratory volume in one second is reduced in the first second forced expiratory volume (FEV1).
One second forced exhalation/forced vital capacity ratio FEV1/forced vital capacity (FVC) is often <60%.
Maximum ventilation (MVV) as a percentage of predicted value <80%.
Increased lung static compliance (Cst) and decreased dynamic compliance (Cdyn).
The decrease in carbon monoxide diffusion amount (DLCO) is important for the diagnosis of obstructive emphysema. According to the degree of decline in FEV1, obstructive emphysema can be classified into grades I, II and III.
4. CT examination of the chest
In particular, thin-layer high-resolution computed tomography (HRCT) can determine the lesions of central lobe or whole lobular emphysema, understand the size and number of large alveolar follicles, estimate the extent of emphysema in non-macrobubble areas, and predict the outcome of surgical treatment. It has a certain meaning, but it should not be used as a routine check.
Diagnosis
Diagnosis and identification of obstructive emphysema
diagnosis
The diagnosis of obstructive emphysema, especially early diagnosis is not easy. It should be combined with medical history, physical signs, chest X-ray examination and pulmonary function test. All patients have a history of urgency, lung function test shows residual gas and residual gas / The total amount of lungs increased, the first second forced expiratory volume/forced lung capacity decreased, the maximum ventilation decreased, the gas distribution was uneven, and the diffusion function was reduced. After bronchodilator treatment, the lung function was not significantly improved, and the diagnosis was established.
Should pay attention to the differential diagnosis of tuberculosis, lung tumor and occupational lung disease, in addition to chronic bronchitis, bronchial asthma and obstructive emphysema are chronic obstructive pulmonary disease, and chronic bronchitis and bronchial asthma can be complicated by obstructive pulmonary qi Swollen, but the three have connections, but also different, can not be equal, chronic bronchitis in the premalignant emphysema is mainly limited to the bronchial, may have obstructive ventilatory disorders, but to a lesser extent, diffuse function is generally normal, bronchial asthma attacks The period is obstructive ventilatory disorder and pulmonary hyperinflation, the gas distribution can be severely uneven, but the above changes are more reversible, better response to inhaled bronchodilators, diffuse dysfunction is not obvious, and bronchial asthma airway responsiveness Significantly increased, lung function fluctuations are also large, which is characterized by it.
Differential diagnosis
Should pay attention to the differential diagnosis of tuberculosis, lung tumor and occupational lung disease, in addition to chronic bronchitis, bronchial asthma and obstructive emphysema are chronic obstructive pulmonary disease, and chronic bronchitis and bronchial asthma can be complicated by obstructive pulmonary qi Swollen, but the three have connections, but also different, can not be equal, chronic bronchitis in the premalignant emphysema is mainly limited to the bronchial, may have obstructive ventilatory disorders, but to a lesser extent, diffuse function is generally normal, bronchial asthma attacks The period is obstructive ventilatory disorder and pulmonary hyperinflation, the gas distribution can be severely uneven, but the above changes are more reversible, better response to inhaled bronchodilators, diffuse dysfunction is not obvious, and bronchial asthma airway responsiveness Significantly increased, lung function fluctuations are also large, which is characterized by it.
