disease | Chronic Bronchitis |
alias | Lao Manzhi, Chronic Bronchitis |
Chronic bronchitis is a chronic nonspecific inflammation of the trachea, bronchial mucosa, and surrounding tissues caused by infectious or non-infectious factors. Its pathological features include hyperplasia of bronchial glands and increased mucus secretion. Clinically, it presents with symptoms such as persistent cough, sputum production, or wheezing for more than three months per year over two consecutive years. Early symptoms are mild, often occurring in winter and alleviating in spring. In advanced stages, inflammation worsens, and symptoms persist year-round regardless of season. Disease progression may lead to complications such as obstructive emphysema and cor pulmonale, severely impacting work capacity and overall health.
bubble_chart Epidemiology
This disease is a common and frequently occurring condition. According to a nationwide survey in China during the 1970s involving over 60 million people, the prevalence rate was 3.82%. The incidence increases with age, reaching as high as 15% or more among individuals over 50 years old. The prevalence of this disease is closely related to smoking, geographical location, and environmental hygiene. Smokers have a significantly higher prevalence rate than non-smokers. The colder climate in northern regions results in a higher prevalence compared to southern areas. Industrial and mining regions with severe air pollution exhibit higher prevalence rates than general urban areas.
The disease cause of chronic bronchitis is extremely complex, and many factors remain unclear to this day. In recent years, the following related factors have been considered.
(1) Air Pollution: Chemical gases such as chlorine, nitrogen oxides, and sulfur dioxide fumes have irritating and cytotoxic effects on the bronchial mucosa. When smoke or sulfur dioxide levels exceed 1,000 µg/m3
(2) Smoking: Smoking is now widely recognized as the most significant disease cause of chronic bronchitis. Smoking shortens and disrupts the cilia of bronchial epithelial cells, impairs ciliary movement, reduces local resistance, weakens the phagocytic and bactericidal functions of alveolar macrophages, and induces bronchial spasms, increasing airway resistance. In 1972, the Shanghai Chronic Bronchitis Prevention and Treatment Collaborative Group surveyed 339 individuals aged 50 and above, finding that the prevalence of chronic bronchitis among smokers was twice that of non-smokers (20.9% vs. 9.7%). Another paired study comparing 303 chronic bronchitis patients and 303 healthy individuals revealed that the smoking rate in the chronic bronchitis group was significantly higher than in the control group.
(3) Infection: Respiratory infections are another major factor in the onset and exacerbation of chronic bronchitis. Domestic and international studies suggest that *Streptococcus pneumoniae*, *Haemophilus influenzae*, and *Moraxella catarrhalis* may be the primary pathogens responsible for acute episodes.
Viruses also play a crucial role in the development and progression of the disease. Viruses isolated during acute stages of chronic bronchitis include rhinoviruses, influenza B virus, parainfluenza virus, myxoviruses, adenoviruses, and respiratory syncytial virus. Viral infections damage respiratory epithelium, facilitating bacterial infections and triggering the onset and recurrence of the disease. The direct relationship between *Mycoplasma pneumoniae* and chronic bronchitis remains unclear.
(5) Other Factors: Besides the above, climate changes—especially cold air—can increase mucus secretion and weaken bronchial ciliary movement. In winter, fluctuations in patients' conditions correlate significantly with temperature and temperature variations. Autonomic dysfunction may also be an intrinsic factor, as most patients exhibit such irregularities. Some patients show hyperactive parasympathetic function and heightened airway reactivity.
In the elderly, declining gonadal and adrenal cortical function, weakened laryngeal reflexes, degraded respiratory defense mechanisms, and impaired monocyte-macrophage system function can also increase susceptibility to chronic bronchitis.
Nutrition also influences bronchitis. Vitamin C deficiency lowers the body's resistance to infection and increases vascular permeability, while vitamin A deficiency weakens the repair function of bronchial mucosal columnar epithelial cells, reduces lysozyme activity, and predisposes individuals to chronic bronchitis.
Whether genetic factors are related to the onset of chronic bronchitis has not been confirmed to date. Severe deficiency of α1-antitrypsin can cause lung qi swelling, but without symptoms of airway lesions, suggesting that it is not directly related to chronic bronchitis.bubble_chart Pathological Changes
The main pathological changes of chronic bronchitis are as follows.
(1) Glandular hyperplasia and hypertrophy, with hyperactive secretion function. In chronic bronchitis, the mucous acini significantly increase, the glandular ducts expand, while the serous and mixed glands correspondingly decrease. Some glands are almost entirely occupied by mucous glands. Goblet cells also show obvious hyperplasia. The Reid index (the ratio of gland thickness to bronchial wall thickness) in chronic bronchitis increases to 0.55–0.79 or more (normal is below 0.4). A higher Reid index indicates more severe inflammation, greater glandular hypertrophy, and narrower bronchial lumens. The hyperplastic and hypertrophic glands exhibit hyperactive secretion, leading to increased mucus production, which results in a higher daily sputum volume in patients.
(2) Changes in the mucosal epithelial cells. Due to recurrent inflammatory episodes, focal necrosis and squamous metaplasia of the epithelium occur. The ciliated epithelial cells are damaged to varying degrees, with shortened, irregular, or sparse and shedding cilia.
(3) Alterations in the bronchial wall. The bronchial wall shows infiltration by various inflammatory cells, congestion, edema, and fibrous hyperplasia. Ulceration occurs in the bronchial mucosa, with granulation tissue hyperplasia. In severe cases, the bronchial smooth muscle and elastic fibers are also damaged, leading to organization and luminal narrowing. A few cases may exhibit atrophy and degeneration of the bronchial cartilage, partially replaced by connective tissue. Mucus plugs may be found within the lumen. Due to mucosal swelling or mucus retention causing obstruction, the local bronchial wall is prone to collapse, distortion, or dilation.
(4) Electron microscopic findings. In chronic bronchitis cases, the following changes can be observed in the alveolar walls: ① Type I alveolar epithelial cells swell and thicken, with swollen mitochondria and dilated endoplasmic reticulum appearing vacuolated. Type II alveolar epithelial cells proliferate. ② The capillary basement membrane thickens, with endothelial cell injury, thrombosis, and luminal fibrosis and occlusion. ③ Diffuse hyperplasia of fibrous tissue in the alveolar walls. These changes are particularly prominent in cases complicated by pulmonary emphysema and cor pulmonale.
[Changes in respiratory function]
In the early stages of chronic bronchitis, the lesions mainly affect small airways with an internal diameter of <2 mm. Clinical symptoms are not obvious, and routine pulmonary function tests are mostly normal, but the closing volume test may show an increase. When the inflammation spreads to larger bronchi, during acute exacerbations, airway narrowing and increased resistance occur. Routine ventilation function tests, such as maximum ventilation volume, forced expiratory volume in 1 second, and maximum mid-expiratory flow rate, all show grade I reduction. The residual volume shows grade I increase, but the vital capacity remains normal. During the remission stage, pulmonary function changes can return to normal. Once complicated by obstructive pulmonary emphysema, the damage to respiratory function is mostly irreversible.
bubble_chart Clinical Manifestations
Some patients have a history of acute respiratory infections such as acute bronchitis, influenza, or pneumonia before the onset of the disease. Patients often develop symptoms during cold seasons, including cough and expectoration, particularly prominent in the morning. The sputum is white, viscous, and frothy, making it difficult to expectorate. During acute respiratory infections, symptoms rapidly worsen. The amount of sputum increases, its viscosity intensifies, or it becomes yellow and purulent, occasionally with blood streaks. After repeated episodes of chronic bronchitis, the reactivity of the vagal receptors in the bronchial mucosa increases, and parasympathetic hyperfunction may occur, leading to hypersensitivity and the onset of wheezing. As the condition progresses, cough and expectoration persist year-round, worsening in autumn and winter. Patients with asthmatic bronchitis often experience asthma-like attacks during symptom exacerbation or secondary infections, with shortness of breath preventing them from lying flat. Dyspnea is generally not prominent, but when complicated by
emphysema, it gradually worsens as the degree of emphysema increases.
Signs: In the early stages, there are often no signs. Sometimes, moist or dry rales can be heard at the base of the lungs. In asthmatic bronchitis, wheezing sounds may be heard after coughing or deep inspiration, and widespread wheezing occurs during attacks. Long-standing cases may show signs of
emphysema.
X-ray findings: In simple chronic bronchitis, X-ray examination may be negative or only reveal thickened lung markings in the lower lobes, or linear shadows, indicative of fibrous tissue proliferation and thickening of the bronchial walls. If peribronchitis is present, spotty shadows may overlap. Bronchography with iodized oil often reveals bronchial deformities, including narrowing, cylindrical dilation, or truncation due to sputum retention. Due to contraction of surrounding scar tissue, bronchi may converge into bundles. Occasionally, small diverticula may be seen on the bronchial walls, representing dilated openings of mucous glands. For clinical diagnosis, fluoroscopy or plain radiography is usually sufficient. Bronchography with iodized oil is reserved for special studies and is not a routine examination.
The diagnosis mainly relies on medical history and symptoms. After excluding other cardiac and pulmonary diseases (such as subcutaneous node, pneumoconiosis, bronchial asthma, bronchiectasis, lung cancer, heart disease, cardiac insufficiency, etc.), a clinical diagnosis can be established if the patient has chronic or recurrent cough, expectoration, or accompanied by wheezing, with symptoms persisting for at least 3 months each year and lasting for two consecutive years or more. If the duration of symptoms each year is less than three months but there is clear objective evidence (such as X-ray, pulmonary function tests, etc.), the diagnosis can also be made.
Based on clinical manifestations, chronic bronchitis is classified into two types: simple type and wheezing type. The former mainly presents with recurrent cough and expectoration; the latter, in addition to cough and expectoration, also exhibits wheezing symptoms accompanied by wheezing sounds.
According to the course of the disease, it can be divided into the late stage [third stage], to guide treatment with a focus.
(1) Acute stage of attack: Refers to the appearance of purulent or mucopurulent sputum within one week, a significant increase in sputum volume, or accompanied by inflammatory manifestations such as fever, or any one of the symptoms of "cough," "sputum," or "wheezing" significantly worsening within one week, or a marked deterioration in severe patients.
(2) Chronic protracted stage: Refers to varying degrees of "cough," "sputum," or "wheezing" symptoms persisting for more than one month.
(3) Clinical stage of remission: After treatment or natural relief, symptoms are basically absent or only occasional mild cough and minimal sputum, lasting for more than two months.
bubble_chart Treatment Measures
(1) Prevention First Smoking is a major cause of chronic bronchitis, and the smoke also harms people around. The dangers of smoking should be widely publicized, and young people should be educated to avoid smoking. At the same time, in response to the disease-causing factors of chronic bronchitis, personal hygiene should be strengthened, including physical, respiratory, and cold-resistance exercises to enhance constitution and prevent common colds. Environmental hygiene should be improved by managing the "three wastes" (waste gas, waste water, and industrial residue) and reducing air pollution to lower the incidence rate.
(2) Treatment During the Stage of Remission The focus should be on enhancing constitution, improving disease resistance, and preventing relapse. Bronchitis vaccine is generally administered before the onset season, with subcutaneous injections once a week. The dose starts at 0.1ml and increases by 0.1–0.2ml each time until reaching a maintenance dose of 0.5–1.0ml. If effective, the treatment should be continued for 1–2 years. Nucleotide injection (culture medium of measles virus vaccine) can be administered intramuscularly or subcutaneously twice a week, 2–4ml each time. Alternatively, BCG polysaccharide injection can be administered intramuscularly three times a week, 1ml each time (containing 0.5mg of BCG extract). Starting medication before the onset season for three consecutive months can reduce the occurrence of common colds and chronic bronchitis attacks. Biostim (a glycoprotein extracted from Klebsiella pneumoniae) is used in an initial 8-day treatment at 2mg/day, followed by a 3-week break; a second 8-day treatment at 1mg/day, followed by a 3-week break; and a third 8-day treatment at 1mg/day, totaling a 3-month course to prevent chronic recurrent respiratory infections.
(3) Treatment During Acute Stage of Attack and Chronic Prolonged Stage The focus should be on controlling infection, dispelling phlegm, and relieving cough. For cases accompanied by wheezing, antispasmodic and anti-asthmatic drugs should be added.
① Antibacterial Treatment: For general cases, common pathogenic bacteria should guide medication selection. Options include compound sulfamethoxazole (SMZ), 2 tablets twice daily; amoxicillin 2–4g/day, divided into 3–4 oral doses; ampicillin 2–4g/day, divided into 4 oral doses; cefalexin 2–4g/day or cefradine 1–2g/day, divided into 4 oral doses; cefuroxime 1g/day or cefaclor 500mg–1g/day, divided into 2–3 oral doses. Alternatively, newer macrolide antibiotics such as roxithromycin 0.3g/day, divided into 2 oral doses, may be chosen. The antibacterial treatment course is generally 7–10 days, with prolonged courses for recurrent infections. If no improvement is seen after three days of treatment, antibiotics should be selected based on sputum culture and drug sensitivity test results.
For severe infections, intravenous drip administration of ampicillin, ciprofloxacin, ofloxacin, amikacin, netilmicin, or cephalosporins may be used. For specific dosages, refer to "Antibacterial Drug Treatment."
② Expectorants and Antitussives: Mucosolvan (ambroxol hydrochloride) 30mg or resolving phlegm tablets (carbocisteine) 500mg can be taken orally three times daily. Bromhexine (Bisolvon) and ammonium chloride brown mixture also have certain expectorant effects. When phlegm is too thick to expectorate, steam inhalation with loquat leaf or ultrasonic nebulization can be used to dilute airway secretions.
For chronic bronchitis, except in cases of irritating dry cough, antitussives should not be used alone, as they may prevent phlegm expulsion and worsen the condition.
(3) Antispasmodic and Antiasthmatic Drugs For asthmatic bronchitis, antispasmodic and antiasthmatic drugs are often selected, such as aminophylline 0.1~0.2g, taken orally three times daily; meptin 50µg, taken orally twice daily; bricanyl 2.5mg, taken orally two to three times daily; compound formula chlorpheniramine tablets, one tablet taken orally three times daily. For chronic bronchitis with reversible obstruction, bronchodilators should be routinely used, such as ipratropium bromide aerosol and bricanyl turbuhaler for inhalation therapy. Paroxysmal cough is often accompanied by varying degrees of bronchospasm, and the use of bronchodilators can alleviate symptoms and facilitate the clearance of sputum.
(1) Obstructive lung qi swelling is the most common complication of chronic bronchitis. Refer to "Obstructive lung qi swelling."
(2) Bronchopneumonia occurs when chronic bronchitis spreads to the peribronchial lung tissue, accompanied by shiver, fever, intensified cough, increased sputum production with purulent characteristics. Total white blood cell count and neutrophil count rise. X-ray examination reveals small speckled or patchy shadows in the lower lung fields.
(3) Bronchiectasis develops from recurrent episodes of chronic bronchitis, leading to bronchial mucosal congestion, edema, ulcer formation, fibrous proliferation of the bronchial wall, and varying degrees of deformation, dilation, or stenosis of the lumen. The dilated portions often exhibit cylindrical changes.
(1) Pulmonary tuberculosis Active pulmonary tuberculosis is often accompanied by symptoms such as low-grade fever, lack of strength, night sweating, and hemoptysis; the severity of cough and sputum production is related to the activity of pulmonary tuberculosis. Chest X-ray can reveal lung lesions, and sputum tuberculosis bacteria tests are positive. In elderly patients with pulmonary tuberculosis, toxic symptoms are often inconspicuous and may go unnoticed for a long time due to being masked by chronic bronchitis symptoms, requiring special attention.
(3) Bronchial asthma The onset typically occurs at a younger age, often with a personal or family history of allergic sexually transmitted diseases. The trachea and bronchi exhibit heightened reactivity to various stimuli, manifesting as widespread bronchospasm and luminal narrowing. Clinically, it presents with paroxysmal dyspnea and cough, with episodes that may be brief or prolonged. Chest percussion reveals hyperresonance, and auscultation shows prolonged expiration accompanied by high-pitched wheezing. In advanced stages, chronic bronchitis often develops. Eosinophils are more abundant in the sputum of bronchial asthma patients but less so in patients with asthmatic bronchitis.
(3) Bronchiectasis This condition mostly occurs in children or young adults, often secondary to measles, pneumonia, or whooping cough, and is characterized by recurrent large amounts of purulent sputum and hemoptysis. Moist rales can be heard in the lower lobes of both lungs. Chest X-ray shows deepened bronchial shadows in the lower lobes, and severe cases may exhibit "tramline" or "ring-like" shadows. Bronchial contrast radiography reveals cylindrical or cystic bronchiectasis.
(4) Heart disease Cough caused by pulmonary congestion is usually dry, with little sputum production. Detailed history-taking may reveal signs of heart disease such as palpitations, shortness of breath, and lower limb edema. Signs, X-ray, and electrocardiogram examinations can aid in differentiation.
(5) Lung cancer This condition predominantly affects males over 40 years of age, particularly long-term smokers, and often presents with blood-streaked sputum and irritating cough. Chest X-ray may show a mass shadow or obstructive pneumonia. A definitive diagnosis can be made through sputum cytology or fiberoptic bronchoscopy.