Chronic obstructive pulmonary disease (COPD)is a heterogeneous lung disease characterized by chronic respiratory symptoms (dyspnea, cough, expectoration) and persistent and progressive airflow limitation caused by abnormal airways (bronchitis, bronchiolitis) and/or abnormal alveoli (emphysema). Irreversible airflow limitation is the key to diagnosis of COPD. After inhaling bronchodilators, a ratio of forced expiratory volume in one second (FEV1) to forced vital capacity (FVC) (FEV1/FVC) < 70% indicates the presence of persistent airflow limitation.
COPD has a close relationship with chronic bronchitis and emphysema. Chronic bronchitis is manifested by cough and expectoration for more than 3 months each year for 2 consecutive years after other known causes of chronic cough are excluded. Emphysema is abnormal and persistent dilation of the distal airspaces of the terminal bronchioles in the lungs, accompanied by the destruction of alveoli and bronchioles, without significant pulmonary fibrosis. When patients with chronic bronchitis and/or emphysema have persistent airflow limitation in pulmonary function tests, they can be diagnosed with COPD; if patients only have chronic bronchitis and/or emphysema without persistent airflow limitation, they cannot be diagnosed with COPD.
Some diseases with known causes or characteristic pathological manifestations can also lead to persistent airflow limitation, such as bronchiectasis, fibrotic lesions of pulmonary tuberculosis, severe interstitial lung disease, diffuse panbronchiolitis, and obliterative bronchiolitis, but they are not COPD.
Etiology and risk factor
The etiology of this disease is not completely clear. It may be the result of long-term interaction between various environmental factors and the body's own factors.
Genetic factor
There is a genetic predisposition to COPD. Severe α1-antitrypsin deficiency is associated with the formation of emphysema in non-smokers. Polymorphisms of certain genes, such as genes encoding MMP12 and GST, may be related to the decline of lung function. Whole-gene scans have shown that α-nicotine acetylcholine receptors and hedgehog-interacting proteins (HHIP) are associated with COPD or lung function. The latest research found 82 gene loci related to COPD. Different genes are associated with different pathological or clinical characteristics of COPD, supporting the presence of heterogeneity in COPD from genetic perspectives.
Age and gender
Age is a risk factor for COPD, and the prevalence of COPD increases with age. Gender differences in COPD prevalence are inconsistently reported; however, it is reported that females are more sensitive to the hazards of tobacco smoke.
Lung growth and development
Direct and indirect exposure to harmful factors during pregnancy, birth, and adolescence can affect lung growth; and poor lung growth is a risk factor for COPD.
Bronchial asthma and airway hyperresponsiveness
Asthma can not only coexist with COPD, but is also a risk factor for COPD. Airway hyperresponsiveness is also involved in the pathogenesis of COPD.
Low body mass index
Low body mass index (BMI) is associated with high prevalence of COPD. There is an interactive effect between cigarette smoking and BMI on COPD.
Tobacco
Cigarette smoking is the most important environmental causative factor of COPD. Compared with non-smokers, smokers have a higher rate of lung function abnormalities, a faster annual decline of forced expiratory volume in one second (FEV1), and an increased risk of death. Passive smoking may also cause respiratory symptoms and the occurrence of COPD. Cigarette smoking in pregnant women may affect fetal development and lung growth in the womb, and may have a certain impact on the immune system function of the fetus.
Fuel fume
Fumes produced by fuels such as firewood, coal, and animal waste contain large amounts of harmful components, such as carbon oxides, nitrogen oxides, sulfur oxides, and unburned hydrocarbon particles and polycyclic organic compounds. Large amounts of smoke produced during combustion may be an important cause of COPD in non-smoking individuals. Indoor air pollution from fumes has a synergistic effect with cigarette smoking. Switching to cleaner fuels and increasing ventilation can slow down the decline of lung function and reduce the risk of COPD.
Air pollution
Particulate matter (PM) and harmful gases, such as sulfur dioxide, nitrogen dioxide, ozone, and carbon monoxide, in air pollution have irritating and cytotoxic effects on bronchial mucosa. When the concentration of PM2.5~ in the air exceeds 35 μg/m3, the risk of COPD is significantly increased. Sulfur dioxide in air contributes to PM, and is positively correlated with the count of acute exacerbations of COPD.
Occupational dust
Long time exposure to high concentration of occupational dust, such as silica, coal dust, cotton dust, and sugar dust, can lead to the occurrence of COPD. Exposure to irritating substances, organic dust, and allergens in the occupational environment can lead to increased airway responsiveness, thereby contributing to COPD.
Infections and chronic bronchitis
Respiratory tract infection is an important factor in the onset and exacerbation of COPD, and viral or bacterial infections are common causes of acute exacerbation of COPD. Recurrent lower respiratory tract infections in childhood are associated with reduced lung function and the development of respiratory symptoms in adulthood. It is observed that chronic bronchitis increases the possibility of COPD and may be related to the number and severity of acute exacerbations.
Socioeconomic status
The incidence of COPD is related to socioeconomic status. There may be some inherent connection between the different levels of indoor and outdoor air pollution, nutritional status, and socioeconomic status.
Pathogenesis
Chronic inflammation of the airways, lung parenchyma, and pulmonary vessels is a characteristic change of COPD. Inflammatory cells such as neutrophils, macrophages, and T lymphocytes are involved in the pathogenesis of COPD. The activation and aggregation of neutrophils play an important role in the inflammatory process of COPD. The release of various bioactive substances such as neutrophil elastase causes chronic mucus hypersecretion and damages the lung parenchyma.
Proteolytic enzymes can damage and destruct the tissues; antiproteases have inhibitory functions on various proteases such as elastase, in which α1-antitrypsin (α1-AT) is the most active. An increase in proteases or a deficiency in antiproteases can lead to structural damage of tissues, resulting in emphysema. Inhalation of harmful gases and substances can lead to an increase in the production or activity of proteases and a decrease in the production of antiproteases or accelerated inactivation of antiproteases; and risk factors such as oxidative stress and cigarette smoking can also reduce the activity of antiproteases. Congenital α1-AT deficiency is more common in individuals of Nordic descent.
Many studies have shown that oxidative stress is increased in patients with COPD. Oxides mainly include superoxide anion, hydroxyl, hypochlorous acid, hydrogen peroxide, and nitric oxide; can directly act on and damage many biochemical macromolecules such as proteins, lipids, and nucleic acids, leading to cellular dysfunction or death; and can also damage the extracellular matrix; leading to protease-antiprotease imbalance. The imbalance promotes inflammatory responses, such as activation of the transcription factor NF-kB, and participate in the transcription of various inflammatory mediators, such as IL-8, TNF-α and inducible nitric oxide synthase (NOS) and cyclooxygenase.
Abnormal lung development, infections, childhood asthma, autonomic dysfunction, malnutrition, and temperature changes may all be involved in the occurrence and development of COPD.
The above mechanisms act together and eventually cause small airway lesions, including small airway inflammation, formation of fibrous tissue in small airways, mucus plugs in small airway lumens, which result in a significant increase in small airway resistance; and emphysema, which reduce the normal tension of alveoli on small airways, resulting in small airways more prone to collapse, and emphysema significantly reduces the elastic recoil of alveoli. The interaction of these small airway lesions and emphysema causes the characteristic persistent airflow limitation of COPD.
Pathology
Characteristic pathological changes of COPD are in the airway, lung parenchyma, and pulmonary vessels. Inflammatory cell infiltration, epithelial damage, and enlarged mucous glands and increased goblet cells resulting in increased mucus secretion are in the central airway. Pathological changes in peripheral small airways include obstruction and structural changes in peripheral small airways (inner diameter <2 mm), airway remodeling caused by stenosis and peritubular fibrosis, and loss of terminal bronchioles and transitional bronchioles. These changes are already present in early stage. Various inflammatory cells, such as macrophages, neutrophils, B cells, and T cells, infiltrating the airway wall and increased mucus secretions blocking the airway lumen cause fixed airway obstruction and airway wall structural remodeling. Emphysema results in destruction of the alveolar septa that surround small airways, weakening the force that keeps the small airways open. The above pathological changes together constitute the pathological basis of airflow limitation in COPD.
The pathological changes of emphysema include overexpansion of the lungs, elasticity attenuation, grayish white or pale appearance, and variously sized bullae on the surface. The destruction of lung parenchyma and the expansion and destruction of respiratory bronchioles can be seen in microscopy, forming mainly centrilobular emphysema. In mild patients, these damages often occur in the upper lungs, but as the disease progresses, they can spread throughout the lungs. Pulmonary vascular changes occur in the early stage. Intimal thickening of the small pulmonary blood vessels in mild to moderate (GOLD 1 - 2) COPD is present. As the disease develops, hyperplasia and hypertrophy of smooth muscle cells and the increase in proteoglycans and collagen further thicken the blood vessel walls. In severe to critical (GOLD 3 - 4) COPD, there are thickening of elastic fibers in the blood vessel wall, proliferation of smooth muscle, infiltration of inflammatory cells in the blood vessel wall, and reduced count of pulmonary capillaries. In the late stage, when secondary pulmonary heart disease occurs, in situ thrombosis of multiple small pulmonary arteries may be seen in some patients.
Table 1 GOLD classification of COPD
Pathophysiology
The characteristic pathophysiological change of COPD is the continuous airflow limitation leading to pulmonary ventilation dysfunction. With the progression of the disease, the elasticity of lung tissue decreases increasingly, alveoli continue to expand and have difficulty in retraction, then the residual air volume and the percentage of residual air volume in total lung volume increase. The aggravation of emphysema leads to the degeneration of numerous capillaries around the alveoli due to the compression of alveolar expansion, resulting in a significant reduction of pulmonary capillaries and a decrease in blood flow between alveoli. At this time, although the alveoli are ventilated, there is no blood perfusion in the alveolar walls, resulting in an increase in the volume of physiological dead space; moreover, in some lung areas, although there is blood perfusion, the alveoli are poorly ventilated and cannot participate in gas exchange, resulting in an increase in functional shunt, thereby causing a mismatch of ventilation and blood flow. Large loss of alveoli and capillaries and a reduction in the diffusion area further lead to disorders in gas exchange function. Ventilation and gas exchange dysfunction cause hypoxia and carbon dioxide retention, and hypoxemia and hypercapnia can occur, eventually resulting in respiratory failure.
Airflow limitation and air trapping
Progressive, irreversible airflow limitation is a core feature of the pathophysiology of COPD, and is manifested by decline of both the ratio of forced expiratory volume in one second (FEV1) to forced vital capacity (FVC) and FEV1, which are associated with increased small airway resistance and decreased alveolar elastic recoil. Airflow limitation results in air trapped in the lungs during expiration, causing lung hyperinflation and increased intrathoracic pressure, leading to decreased alveolar ventilation and abnormal ventricular filling, thereby leading to exertional dyspnea and decreased exercise tolerance. Hyperinflation can occur in the early stage of COPD and is the main cause of exertional dyspnea.
Abnormal gas exchange
There are multiple mechanisms underlying gas exchange abnormalities in COPD. Airflow limitation causes hyperinflation and increased lung capacity, reducing inspiratory muscle strength. Increased airway resistance leads to increased respiratory load. The combined effect of the two factors can lead to an imbalance between respiratory load and muscle strength, and weakened driving forces for ventilation result in significantly decreased alveolar ventilation. Extensive destruction of lung parenchyma and reduction of pulmonary capillary beds result in imbalance of ventilation/blood flow ratio and further deterioration of gas exchange, so hypoxemia occurs and is often accompanied by hypercapnia. This series of pathophysiological changes will be further disrupted during acute exacerbation of COPD, leading to severe dyspnea in patients.
Mucus hypersecretion and ciliary dysfunction
Tobacco smoke and other harmful substance stimulation result in elevated count of goblet cells and enlarged submucosal glands, leading to mucus hypersecretion. Cigarette smoking can cause squamous metaplasia of columnar epithelium and short and irregular cilia, resulting in ciliary dyskinesia. Mucus hypersecretion and ciliary dysfunction are important causes of chronic cough and expectoration. However, not all patients with COPD have mucus hypersecretion, and mucus hypersecretion is not necessarily accompanied by airflow limitation.
Pulmonary hypertension
With the progression of COPD, chronic hypoxia leads to hypoxic contraction of pulmonary arterioles, endothelial cell dysfunction, and smooth muscle hypertrophy and proliferation, contributing to the occurrence and development of hypoxic pulmonary hypertension. Subsequently, chronic pulmonary heart disease. and right heart failure occur, suggesting a poor prognosis.
Clinical manifestations
Main clinical manifestations are chronic cough, expectoration, and dyspnea. There may be not obvious symptoms in the early stage. Cough and expectoration usually occur in the early stage, while dyspnea is the main manifestation in the late stage.
Cough occurs slowly and persists for many years, predominantly in the morning and at night. Expectoration is often accompanied by cough, mostly in the morning. The sputum is often white, serous mucus. In acute exacerbation, the sputum can be mucopurulent. Tachypnea or dyspnea only occurs during exertion in the early stage, and is gradually exacerbated. As a result, dyspnea occurs during daily activities and even at rest. Dyspnea on exertion is the typical symptom of COPD. Evident chest tightness and wheezing are common in acute exacerbation.
Inspection and palpation reveal increased anteroposterior diameter of the thorax, widened infrasternal angle, hypopnea, increased respiratory frequency, prolonged expiratory phase, and auxiliary respiratory muscles, such as scalenes and sternocleidomastoid muscles, involved in respiration. Paradoxical respiration can occur in severe patients. Some patients adopt pursed-lip breathing or forward leaning position or both during exacerbation. Cyanosis may be seen when complicated by hypoxemia, and heart lifting sensation may be palpable.
Percussion of the chest may reveal hyperresonance, decreased area of cardiac dullness, and lowered lung-liver border, which are caused by pulmonary hyperinflation.
Auscultation reveals reduced breath sounds in both lungs, prolonged expiration, dry crackles or wheezing and/or moist crackles, distant heart sounds, and loud and clear subxiphoid heart sounds.
In addition, when complicated by cor pulmonale, patients may present with lower limb edema, ascites, and liver enlargement and tenderness. When complicated by pulmonary encephalopathy, neurological pathological signs may occasionally be elicited.
Complications
Right heart insufficiency
When COPD is complicated by decompensation of chronic pulmonary heart disease, systemic circulation congestion-related symptoms such as anorexia, abdominal distension, and lower limb or systemic edema may occur.
Respiratory failure
It is more common in patients with severe COPD or acute exacerbation. Due to severe damage to ventilatory function, apparent hypoxemia and carbon dioxide retention (type II respiratory failure) occur, and patients may have obvious cyanosis and severe dyspnea. When carbon dioxide is severely retained and respiratory acidosis is decompensated, patients may present symptoms of pulmonary encephalopathy such as strange behavior, delirium, hypersomnia, and even coma.
Spontaneous pneumothorax
It is characterized by sudden exacerbation of dyspnea, chest tightness, and/or thoracodynia, with or without cyanosis.
Laboratory and auxiliary examinations
Pulmonary function test
Pulmonary function test includes FEV1, ratio of FEV1 to FVC (FEV1/FVC), total pulmonary capacity, and diffusing capacity, which are helpful for disease assessment and differential diagnosis. FEV1/FVC < 70% after inhalation of bronchodilator indicates the presence of persistent airflow limitation and is the diagnostic criteria of COPD. In clinical practice, in order to reduce overdiagnosis, if FEV1/FVC is between 68% and 70%, it is recommended to reexamine whether FEV1/FVC < 70% is still present in 3 months. Pulmonary hyperinflation caused by airflow limitation increases total lung capacity (TLC), residual volume (RV), functional residual capacity (FRC), and ratio of residual volume to total lung capacity (RV/TLC), but decreases vital capacity (VC). Inspiratory volume (IC) is the sum of tidal volume and inspiratory reserve volume. In COPD, the decrease of IC is associated with the increase of end-expiratory lung volume, which can be a simple assessment index of changes in lung volume. The ratio of inspiratory volume to total lung capacity (IC/TLC) can reflect the degree of dyspnea in COPD and predict the risk of death. Destruction of the alveolar septa and loss of the pulmonary capillary beds can impair the diffusion function and reduce the diffusing capacity of lungs for carbon monoxide (DLCO).
Chest x-ray
There may be no obvious changes in chest x-ray in the early stage of COPD, and then non-characteristic changes such as increased, disordered lung markings may occur. The main x-ray sign is pulmonary hyperinflation manifested by hyperlucent lung fields, decreased peripheral markings, enlarged anteroposterior diameter of the chest, flattened rib orientation, flattened diaphragm, and pendulous heart. In severe patients, imaging changes of pulmonary bullae are present. When COPD is complicated by pulmonary hypertension and pulmonary heart disease, chest x-ray findings include dilation of the right lower pulmonary artery trunk with a transverse diameter ≥ 15 mm or a ratio of the right lower pulmonary artery transverse diameter to the tracheal transverse diameter ≥ 1.07 or dynamic observation of the increased width of the right lower pulmonary artery trunk > 2 mm; prominent pulmonary artery segment or its height ≥ 3 mm; dilated central pulmonary artery and thinned peripheral branches forming pulmonary knuckle sign; significantly bulged cone (right anterior oblique view 45°) or its height ≥ 7 mm; and right ventricular enlargement.
Chest CT
High-resolution CT has high sensitivity and specificity in distinguishing centrilobular and panlobular emphysema and determining the size and count of bullae, and is often used for differential diagnosis and pretreatment evaluation of non-drug treatment. It has certain value in predicting the effect of bullae resection or surgical volume reduction surgery. Under the assistance of high-resolution CT, the calculation of indicators such as emphysema index, airway wall thickness, and functional small airway lesions is helpful for early diagnosis and phenotypic assessment of COPD.
Saturation of peripheral oxygen (SpO2) and arterial blood gas analysis
When clinical symptoms suggest respiratory failure or right heart failure, SpO2 should be monitored. If SpO2 < 92%, arterial blood gas analysis should be performed. The diagnostic criteria for arterial blood gas analysis of respiratory failure are PaO2 < 60 mmHg (1 mmHg = 0.133 kPa) when breathing air at sea level at rest, with or without PaCO2 > 50 mmHg。
Electrocardiogram and echocardiogram
The electrocardiogram of COPD complicated by chronic pulmonary hypertension or chronic cor pulmonale may reveal the mean frontal plane electrical axis ≥ +90°; R/S ≥ 1 in lead V1; severe clockwise rotation (R/S ≤ 1 in lead V5); RV1 + SV5 ≥ 1.05mV; R/S or R/Q ≥ 1 in lead aVR; QS, Qr or qr in lead V1 - V3 (resembling myocardial infarction); and P pulmonale. Echocardiogram of COPD complicated by chronic cor pulmonale can reveal right ventricular outflow tract inner diameter ≥ 30 mm; right ventricular inner diameter ≥ 20 mm; right ventricular anterior wall thickness ≥ 5 mm or increased anterior wall pulsation amplitude; left and right ventricular inner diameter ratio < 2; right pulmonary artery inner diameter ≥ 18 mm or pulmonary artery trunk ≥ 20 mm; right ventricular outflow tract/left atrial inner diameter > 1.4; and signs of pulmonary hypertension in the pulmonary valve curve (A wave declined and flattened or < 2 mm, or midsystolic closure sign).
Routine blood tests
Due to long-term hypoxemia, some patients may present with significantly increased peripheral blood hemoglobin, erythrocytes, and hematocrit; and some patients may be with anemia.
Diagnosis
On the basis of a history of exposure to risk factors, symptoms, signs, and pulmonary function test, as well as exclusion of other diseases that may cause similar symptoms and persistent airflow limitation, the disease can be diagnosed.
Pulmonary function test showing persistent airflow limitation is a prerequisite for the diagnosis of COPD. After inhalation of bronchodilators, FEV1/FVC < 70% clearly indicates the presence of persistent airflow limitation.
Differential diagnosis
Bronchial asthma
Bronchial asthma is characterized by early onset (usually in childhood), large daily symptom variation, obvious symptoms at night and in the morning, often accompanied by a history of allergies, rhinitis, eczema, family history, and obesity
Congestive heart failure
Congestive heart failure is manifested by cardiomegaly and pulmonary edema in chest x-ray, and restrictive ventilation disorders rather than airflow limitation in pulmonary function test.
Bronchiectasis
Bronchiectasis presents with repeated purulent expectoration or hemoptysis, often accompanied by bacterial infection, coarse and moist crackles, and clubbed fingers, as well as bronchial dilatation and tube wall thickening in the chest x-ray or chest CT.
Pulmonary tuberculosis
Pulmonary tuberculosis is characterized by onset in all ages, high incidence in endemic areas, and pulmonary infiltrative lesions or nodular, cavitary lesions in chest x-ray.
Obliterative bronchiolitis
Obliterative bronchiolitis, also known as bronchiolitis obliterans, is characterized by onset in young individuals, absence of cigarette smoking history, with or without a history of rheumatoid arthritis or acute smog exposure, as well as hypodense opacity in expiratory CT
Diffuse panbronchiolitis
Diffuse panbronchiolitis mainly occurs in Asian populations, and almost all patients have chronic sinusitis. Chest x-ray and high-resolution CT show diffuse, central, lobular, nodular opacities and hyperinflation sign
Treatment
Inhalation device selection
In patients with sufficient inspiratory flow rate (peak inspiratory flow rate ≥ 30 L/min) and good hand-mouth coordination, one of dry powder inhaler (DPI), pressurized metered dose inhaler (pMDI) (including traditional pMDI and co-suspension pMDI), and soft mist inhaler (SMI) can be selected. In patients with poor hand-mouth coordination, the recommended inhalation device is DPI, pMDI + spacer, or SMI. In patients with insufficient inspiratory flow rate (peak inspiratory flow rate < 30 L/min) but with good hand-mouth coordination, the recommended inhalation device is SMI or pMDI. In patients with poor hand-mouth coordination, the recommended inhalation device is pMDI + spacer, SMI, or nebulizer. In patients who require mechanical ventilation, the recommended inhalation device is nebulizer, pMDI, or SMI.
In inhalation therapy, it should be considered that COPD patients have excessive mucus secretion, which may block the small airways and affect the entry of drug particles into the small airway effector site. Therefore, before inhalation therapy, airway clearance can be performed. It is recommended to cough actively before inhaling the drug. If there is sputum, it is necessary to clear the sputum before inhaling the drug.
Recommendation of initial treatment
Depending on the severity, the initial treatment for patients with stable COPD can be divided into 4 groups.
Group A treatment is a short-acting or long-acting bronchodilator.
Group B treatment is a long-acting bronchodilator, or long-acting antimuscarinic (LAMA) + long-acting β2 receptor agonists (LABA) If COPD assessment test (CAT) > 20.
Group C treatment is LAMA or inhaled corticosteroids (ICS) + LABA.
Group D treatment is LAMA, LAMA+LABA, ICS+LABA, or ICS+LAMA+LABA.
If CAT > 20, combination therapy of two bronchodilators is preferred. In patients with blood eosinophil count ≥ 300/μl or with asthma, combination therapy containing ICS is recommended.
Table 2 Common medications for COPD
General measures
General measures are an important part of the treatment of stable COPD, and play a synergistic role with medication treatment, including patient management, respiratory rehabilitation, home oxygen therapy, home non-invasive ventilation, vaccination, airway intervention, and surgical treatment.
Respiratory rehabilitation
Respiratory rehabilitation can relieve dyspnea symptoms, improve exercise tolerance, improve quality of life, reduce anxiety and depression symptoms, and reduce the risk of re-hospitalization within 4 weeks after acute exacerbation. In patients with dyspnea, respiratory rehabilitation should be recommended. Relative contraindications include unstable angina, severe cardiac dysrhythmia, cardiac insufficiency, uncontrolled hypertension, neuromuscular diseases, arthropathy, peripheral vascular diseases, and severe cognitive dysfunction or mental disorders. Exercises include aerobic exercises, resistance training, balance and flexibility exercises, and respiratory muscle training.
Oxygen therapy
Long-term oxygen therapy (LTOT) is generally performed using nasal cannula with a flow rate of 1.0 - 2.0 L/min for >15 h/d.
Stable patients receiving LTOT have one of the following characteristics:
- PaO2 ≤ 7.3 kPa (55 mmHg), or SaO2 ≤ 88%, with or without 2 episodes of hypercapnia in 3 weeks
- PaO2 = 7.3 - 8.0 kPa (55 - 60 mmHg), pulmonary hypertension, peripheral edema (congestive heart failure), or polycythemia (hematocrit > 55%).
After initiation of LTOT, the efficacy should be reevaluated within 60 - 90 days to determine whether oxygen therapy is effective and whether continued treatment is needed. The goal of long-term oxygen therapy is to achieve PaO2 ≥ 60 mmHg and/or SaO2 ≥ 90% in patients at sea level and in a resting state, maintaining the function of important organs and ensuring oxygen supply to peripheral tissues.
Home non-invasive positive pressure ventilation
In patients with severe COPD and with severe carbon dioxide retention (PaCO2 ≥ 52 mmHg, pH>7.30), home non-invasive positive pressure ventilation (hNPPV) can improve symptoms and reduce the risk of hospitalization and mortality, and is particularly suitable for patients with obstructive sleep disorders.
Vaccination
Vaccination is an effective treatment to prevent infection with corresponding pathogens. Influenza vaccination can reduce the severity and mortality of COPD patients. Vaccination with 23-valent pneumococcal polysaccharide vaccine (PPSV23) can reduce the incidence of community-acquired pneumonia in COPD patients under age 65. In COPD patients, particularly age > 65, annual influenza vaccination and pneumococcal vaccination every 5 years are recommended. In COPD patients who have never received diphtheria vaccination, it is recommended to receive a booster shot to prevent pertussis, diphtheria, and tetanus.
Interventional treatment
In order to reduce complications and mortality of lung volume reduction surgery, bronchoscopic lung volume reduction (BLVR) is introduced. The common clinical application is endobronchial valve (EBV) therapy. EBV is a one-way valve that allows the residual air in the target lobes to be discharged, thereby causing atelectasis and achieving lung volume reduction. EBV treatment can improve lung function, dyspnea, exercise capacity, and life quality. The prerequisite is absence of interlobar bypass ventilation in the target lobe. Common complications include pneumothorax, valve migration, and acute exacerbation of COPD.
Surgical intervention
In COPD patients, if the progression cannot stop after prompt and adequate medical treatment, including smoking cessation, adequate bronchodilator and hormone inhalation, rehabilitation exercises, and long-term oxygen therapy; lung volume reduction surgery is contraindicated; or the disease progresses after lung volume reduction surgery; lung transplantation can be considered. The perioperative mortality of lung transplantation is 8% - 9% at 3 months, and the average survival time is 7.1 years.
Lung volume reduction surgery (LVRS) is a treatment by surgically removing part of the emphysematous lung tissue. Indications for LVRS include age < 75, smoking cessation for more than 6 months, severe dyspnea after optimal medical medication and rehabilitation treatment, pulmonary function test showing obvious obstructive ventilation dysfunction (FEV1 < 45% of the predicted value), diffusing capacity of the lungs for carbon monoxide (DLCO) > 20%, evidence of air retention in lung capacity test (including RV% > 150% of the predicted value, TLC > 120% of the predicted value, RV/TLC > 60%), chest CT showing areas of hyperventilation and relatively normal lung tissue, and 6-minute walking distance > 140 m after rehabilitation training. Contraindications include FEV1 < 20% of the predicted value; DLCO < 20% of the predicted value, and homogeneous emphysema.
Prevention
Smoking cessation is the most important measure to prevent COPD, and smoking cessation at any stage of the disease helps prevent the occurrence and progression. Control of environmental pollution and reduced inhalation of harmful gases or particles are also essential. Respiratory infections in infants and children should be properly prevented and treated. Influenza vaccine, pneumonia vaccine, anabacteria, and bacillus Calmette-Guérin polysaccharide nucleic acid may be beneficial in preventing recurrent infections in COPD patients. In individuals at high risk of COPD, lung function monitoring should be conducted regularly to detect COPD, and prompt intervention is needed.