I. Epidemiology.
Chronic obstructive pulmonary disease (chronicobstructivepulmonarydisease,COPD) is a preventable and treatable common disease characterized by persistent airflow limitation. COPD has become an important public health problem that affects human health because of its high prevalence, high mortality rate and high socioeconomic burden. The epidemiological survey in China shows that the prevalence of COPD in people over 40 years old is 8.2%, which is a very high prevalence rate. Guo Xinmei, Department of Internal Tuberculosis, Shandong Chest Hospital
Second, the pathogenic factors.
Risk factors for COPD include individual susceptibility factors as well as environmental factors, both of which influence each other. Individual factors: some genetic factors can increase the risk of COPD development. Known genetic factors are α1-antitrypsin deficiency. Bronchial asthma and airway hyperresponsiveness are risk factors for COPD, and airway hyperresponsiveness may be related to certain genetic and environmental factors of the body. Environmental factors: 1. Smoking: Smoking is an important pathogenic factor for COPD. Passive smoking may also lead to respiratory symptoms and the occurrence of COPD. 2. Occupational dust and chemical substances: When the concentration of occupational dust and chemical substances (smoke, allergens, industrial waste gas and indoor air pollution, etc.) is too large or the exposure time is too long, it can lead to the occurrence of COPD unrelated to smoking. Exposure to certain specific substances, irritants, organic dusts and allergens can increase airway reactivity.3. Air pollution: Chemical gases such as chlorine, nitrogen oxide, sulfur dioxide, etc., have an irritating and cytotoxic effect on the bronchial mucosa. Other dusts such as silica, coal dust, cotton dust, cane dust, etc. also stimulate the bronchial mucosa, so that the airway clearance function suffers damage, creating conditions for bacterial invasion. Large amounts of fumes from cooking and soot from biofuels are associated with the onset of COPD, and indoor air pollution from biofuels may have a synergistic effect with smoking.4. Infections: Respiratory infections are another important factor in the onset and exacerbation of COPD, including bacterial and viral infections.
III. Diagnosis
1, medical history features: COPD disease process should have the following characteristics: (1) smoking history: most have a long history of smoking in larger quantities. (2) Occupational or environmental harmful substances exposure history: such as a longer-term dust, smoke, harmful particles or harmful gas exposure history. (3) Family history: COPD has a tendency to cluster in families. (4) Age of onset and season of prevalence: most of the disease develops after middle age, and the symptoms occur in the cold season of autumn and winter, often with a history of recurrent respiratory infections and acute exacerbations. As the disease progresses, acute exacerbations become more and more frequent. (5) History of chronic pulmonary heart disease: hypoxemia and (or) hypercapnia in late COPD can be complicated by chronic pulmonary heart disease and right heart failure.
2. Symptoms: (1) Chronic cough: usually the first symptom. Initially, the cough is intermittent, heavier in the morning, and later in the morning and evening or throughout the day, but the cough is not significant at night. In a few cases, the cough is not accompanied by sputum. In some cases, the cough is not accompanied by sputum, but there is no coughing symptom although there is obvious airflow restriction. (2) Coughing sputum: after coughing, a small amount of mucus sputum is usually coughed up, more in some patients in the early morning; when combined with infection, the sputum volume increases, often with purulent sputum. (3) Shortness of breath or dyspnea: It is the hallmark symptom of COPD and the main cause of anxiety in patients. (4) Wheezing and chest tightness: are not specific symptoms of COPD. Some patients, especially severe patients, have wheezing; tightness in the chest usually occurs after exertion and is associated with respiratory effort and capacitive contraction of intercostal muscles. (5) Systemic symptoms: During the clinical course of the disease, especially in more severe patients, systemic symptoms may occur, such as weight loss, loss of appetite, peripheral muscle atrophy and dysfunction, mental depression and/or anxiety. When combined with infection, coughing up bloody sputum or hemoptysis may occur.
3. Signs: Early signs of COPD may not be obvious. As the disease progresses, the following signs are often present: (1) visual and palpation: abnormal thoracic morphology, including excessive expansion of the chest, increased anterior and posterior diameters, widening of the inferior sternal angle (superior abdominal angle) under the glabella and abdominal bulging, etc.; common shallow breathing, increased frequency, auxiliary respiratory muscles participate in respiratory movements, and in severe cases, contradictory thoracoabdominal movements are seen; anterior sitting position is often adopted when dyspnea worsens; mucous membrane and skin cyanosis may appear in hypoxemia The lower limb edema and liver enlargement are seen in those with right heart failure. (2) Auscultation: The lung may be hyperclear on auscultation due to the narrowing of the cardiac turbid border and the lowering of the lung-hepatic border due to lung hyperinflation. (3) Auscultation: Breath sounds in both lungs may be reduced, the expiratory phase may be prolonged, and dry stalls may be heard during calm breathing.
4. Pulmonary function tests: Pulmonary function measurements are the gold standard for the diagnosis of COPD. A person with FEV1/FVC% <70% after inhalation of bronchodilator can be determined to have airflow limitation that is not fully reversible. Peak expiratory flow rate (PEF) and maximum expiratory flow-volume curve (MEFV) can also be used as reference indicators of airflow limitation, which can lead to hyperinflation of the lungs, resulting in increased total lung volume (TLC), functional residual volume (FRC), and residual volume (RV), and decreased spirometry (VC), with TLC increasing to a lesser extent than RV, resulting in increased RV/TLC. The ratio of DLCO to alveolar ventilation (VA) (DLCO/VA) is more sensitive than that of DLCO alone. Deep inspiratory volume (IC) is the sum of tidal volume and compensatory inspiratory volume. IC/TLC is an indicator of lung hyperinflation, which has significance in reflecting the degree of dyspnea in COPD and even the survival rate of COPD.
5, chest X-ray examination: COPD early X-ray chest film can be no obvious changes, later appear lung texture, disorder and other non-characteristic changes; the main X-ray signs for lung hyperinflation: lung volume increases, the anterior and posterior diameter of the thoracic cavity grows, the ribs flatten, lung field translucency increases, the diaphragm position is low and flat, the heart overhang is narrow, the pulmonary hilar vascular texture is stump-like, the peri-pulmonary vascular texture is slender and sparse, sometimes visible Pulmonary blister formation is sometimes seen. In case of pulmonary hypertension and pulmonary heart disease, in addition to x-ray signs of right heart enlargement, there may be conical expansion of the pulmonary artery, enlargement of the hilar vascular shadow and widening of the right lower pulmonary artery.
6.CT examination of the chest: CT examination is generally not used as a routine examination. However, CT examination is useful in differential diagnosis. High-resolution CT (HRCT) has high sensitivity and specificity in identifying lobar-centered or whole lobar emphysema and determining the size and number of pulmonary blisters, and is of some value in anticipating the effect of pulmonary blister resection or surgical reduction surgery, etc.
7, blood gas examination: When FEV1<40%expected value or COPD patients with respiratory failure or right heart failure should have blood gas examination. Blood gas abnormalities first present as mild to moderate hypoxemia. As the disease progresses, hypoxemia gradually worsens, and even respiratory failure and hypercapnia appear.
8, other laboratory tests: PaO2<55mmHg, hemoglobin and erythrocytes can be increased, and erythrocyte pressure product >55% can be diagnosed as erythrocytosis. In case of co-infection, a large number of neutrophils can be seen in sputum smear, and various pathogenic bacteria can be detected in sputum culture.
IV. Disease staging and treatment
(A) Treatment of stable stage
1.Education and management
The main contents include: (1) educate and urge patients to quit smoking, the only measures that have so far proved to be effective in slowing down the progressive decline of lung function are smoking cessation; (2) make patients understand the pathophysiology and clinical basics of COPD; (3) master the general and some special treatment methods; (4) learn self-control techniques, such as abdominal breathing and lip retraction breathing exercises; (5) understand the timing of hospital visits ; (6) regular follow-up management by community doctors.
2.Control occupational or environmental pollution: avoid or prevent dust, fumes and harmful gas inhalation.
3.Medication
(1) Bronchodilator: It is the main treatment measure to control the symptoms of COPD. Short-term on-demand application can relieve symptoms, long-term regular application can prevent and reduce symptoms and increase exercise endurance, but cannot make all patients’ FEV1 improve. Compared with oral medications, inhalation agents have fewer adverse effects and are therefore mostly preferred for inhalation therapy. The main bronchodilators are β2 agonists, anticholinergics and methylxanthines, which are selected according to the action of the drug and the patient’s response to treatment. The combination of drugs with different mechanisms of action and duration of action can enhance the bronchodilator effect and reduce adverse effects.
(2) Glucocorticoids: Long-term regular inhaled glucocorticoids are indicated for COPD patients with FEV1<50%expected values (classes III and IV) and with clinical symptoms and recurrent exacerbations. This treatment may reduce the frequency of acute exacerbations and improve quality of life. Combined inhaled glucocorticoids and β2 agonists are more effective than each alone, and long-term oral glucocorticoid therapy is not recommended for patients with COPD.
(3) Other drugs: (1) Expectorants (mucolytics): The application of expectorants seems to be beneficial to airway drainage and improve ventilation, but except for a few patients with mucous sputum, the effect is not very precise in general. (2) Antioxidants: Application of antioxidants such as N-acetylcysteine may reduce the frequency of recurrent disease exacerbations. However, the results of long-term, multicenter clinical studies are still lacking, and rigorous clinical studies are needed in the future. (3) Immunomodulators: may have a role in reducing the severity of acute exacerbations of COPD. However, it has not been proven and is not recommended for routine use. (4) Vaccines: Influenza vaccine may reduce the severity and death of COPD patients and may be given once (fall) or twice (fall and winter) per year. Pneumococcal vaccine, which has been used in COPD patients, lacks strong clinical observation data. (5) Chinese medicine treatment: dialectical treatment is the principle of Chinese medicine treatment, and the treatment of COPD should be carried out according to this principle. In practice, we have experienced that certain Chinese medicines have the effects of expectoration, bronchodilatation and immunomodulation, which are worthy of in-depth study.
4.Oxygen therapy
Long-term home oxygen therapy in the stable stage of COPD can improve the survival rate for patients with chronic respiratory failure. Long-term home oxygen therapy should be applied in patients with grade IV, i.e., very severe COPD, with the following specific indications: (1) PaO2 ≤ 55 mmHg or arterial oxygen saturation (SaO2) ≤ 88%, with or without hypercapnia. (2) PaO255-60mmHg, or SaO2<89% with pulmonary hypertension, heart failure edema, or erythrocytosis (erythrocyte ratio >55%). Long-term home oxygen therapy is usually oxygen inhalation via nasal cannula with a flow rate of 1.0-2.0L/min and oxygen duration >15h/d.
5.Rehab therapy
Rehabilitation therapy can improve the mobility and quality of life of patients with progressive airflow limitation, severe dyspnea and little activity, and is an important treatment measure for COPD patients. It includes respiratory physiological treatment, muscle training, nutritional support, psychiatric treatment and education and other measures.
6.Surgical treatment
Pulmonary maculoplasty: In patients with indications, it can reduce the degree of dyspnea and improve the lung function after surgery. Preoperative chest CT examination, arterial blood gas analysis and comprehensive evaluation of respiratory function are very important for deciding whether to operate.
Lung decompression: It is performed by removing part of the lung tissue to reduce lung overinflation, improve respiratory muscle work, and improve exercise capacity and health, but it does not prolong the patient’s life.
Lung transplantation: For patients with advanced COPD who are selected appropriately, lung transplantation can improve the quality of life and lung function, but it is technically demanding and expensive, so it is difficult to promote its application.
(B) Treatment of acute exacerbation
1, drug therapy: acute exacerbation of drug therapy includes three major categories: bronchodilators, systemic glucocorticoids and antibiotics. Single inhalation short-acting β2 agonist, or short-acting β2 agonist and short-acting anticholinergic drugs combined inhalation, is usually the preferred bronchodilator in acute exacerbation. These drugs can improve symptoms and FEV1, and there is no difference between MDI and nebulized inhalation, but the latter may be more appropriate for more severe patients. It is uncertain whether long-acting bronchodilators combined with inhaled glucocorticoids are more effective in acute exacerbations. Theophylline is only suitable for patients with poor results of short-acting bronchodilators, and adverse effects are more common. Systemic glucocorticoids and antibiotics can shorten the recovery time, improve pulmonary function (FEV1) and arterial partial pressure of oxygen (PaO2), reduce the risk of early relapse, reduce the probability of treatment failure and shorten the hospital stay. Oral prednisone 30-40 mg/d for 10-14 d is recommended, and nebulized inhalation budesonide is also an option. Antimicrobial drugs are recommended when AECOPD has three symptoms, namely dyspnea, increased sputum, and purulent sputum, and also when only two symptoms are present and one of them is purulent sputum, including patients who are critically ill and require mechanical ventilation. The type of antimicrobial drug should be selected according to the local bacterial resistance. The recommended course of treatment is 5-7 d.
2.Oxygen therapy: It is an important treatment for acute exacerbation of hospitalization, adjusting and maintaining oxygen saturation 88%-92% according to the patient’s blood oxygen condition.
3.Mechanical ventilation
(1) Non-invasive ventilation: It can improve carbon dioxide retention, reduce respiratory rate and dyspnea, shorten hospital stay, and reduce death and intubation. Indications: At least one of the following conditions is met: respiratory acidosis (arterial blood pH ≤ 7.35 and/or PaCO2 > 45 mmHg); severe dyspnea combined with clinical symptoms, suggesting respiratory muscle fatigue; increased respiratory work; for example, the application of assisted respiratory muscle breathing, the emergence of thoracoabdominal contradictory movements; or contraction of intercostal muscles.
(2) Invasive ventilation: It can reduce the respiratory rate, improve PaO2, PaCO2 and pH, reduce mortality and reduce the risk of treatment failure. The indications for invasive ventilation are as follows: intolerance to NIV or failure of NIV treatment (or inappropriate for NIV), respiratory or cardiac arrest, apnea with loss of consciousness, impaired mental status, severe mental disorder requiring sedation, massive inhalation, prolonged failure to expel respiratory secretions, heart rate <50 beats/min with loss of consciousness, severe hemodynamic instability, failure to respond to fluid therapy and Vasoactive drugs, severe ventricular arrhythmias, life-threatening hypoxemia
(iii) Treatment of comorbidities
”COPD and comorbidities” are mainly cardiovascular disease, osteoporosis, anxiety and depression, lung cancer, infections, metabolic syndrome and diabetes mellitus, etc. COPD often exists in combination with other diseases and can have a significant impact on disease progression. The presence of comorbidities does not require a change in the treatment of COPD, which can occur in patients with COPD regardless of the severity of the disease. The treatment of comorbidities can be based on the principles of treatment for the respective disease.