Chronic bronchitis is a chronic, nonspecific inflammation of the mucosa of the trachea, bronchi, and surrounding tissues. Clinically, it is characterized by cough and expectoration, sometimes accompanied by wheezing. The condition is diagnosed when symptoms persist for at least 3 months per year for 2 consecutive years or longer, after excluding other diseases that may cause similar symptoms of cough, expectoration, and wheezing.
Etiology and Pathogenesis
The exact cause of chronic bronchitis is not fully understood. It is thought to result from the long-term interaction of various environmental and host factors.
Smoking
Smoking is the most significant environmental risk factor. Smokers are 2-8 times more likely to develop chronic bronchitis than non-smokers. The earlier one starts smoking, the longer the duration of smoking, and the greater the quantity smoked, the higher the risk of developing the disease. Harmful chemicals in tobacco, such as tar, nicotine, and hydrogen cyanide, exert multiple damaging effects, including:
- Damage to airway epithelial cells and impairment of ciliary movement, reducing airway clearance.
- Hypertrophy and hyperplasia of bronchial mucus glands and goblet cells, leading to increased mucus secretion.
- Stimulation of the parasympathetic nervous system, causing bronchial smooth muscle contraction and increased airway resistance.
- Increased production of oxygen free radicals, inducing neutrophils to release proteases, which destroy elastic fibers in the lungs and contribute to the development of emphysema.
Occupational/Environmental Dust
Prolonged exposure to occupational or environmental dust, fumes, allergens, or other harmful particles at high concentrations can promote the onset of chronic bronchitis.
Air Pollution
Pollutants such as PM2.5 and harmful gases such as sulfur dioxide, nitrogen dioxide, and chlorine can damage airway mucosal epithelial cells, impair ciliary clearance, and increase mucus production, creating conditions conducive to bacterial infections.
Infectious Factors
Infections caused by viruses, mycoplasma, or bacteria are significant contributors to the development and progression of chronic bronchitis. Common viral pathogens include influenza viruses, rhinoviruses, adenoviruses, and respiratory syncytial viruses. SARS-CoV-2 (the novel coronavirus) is also a contributing factor. Bacterial infections often follow viral infections, with common pathogens including Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus. These infectious agents cause damage to the tracheal and bronchial mucosa, leading to chronic inflammation.
Other Factors
Host factors such as immune dysfunction, airway hyperresponsiveness, autonomic nervous system dysfunction, aging, and environmental factors like climate changes are also associated with the development and progression of chronic bronchitis. For instance, older individuals with reduced adrenal cortical function, impaired cellular immunity, and decreased lysozyme activity are more prone to recurrent respiratory infections. Cold air can stimulate increased mucus secretion, weaken ciliary movement, constrict mucosal blood vessels, and cause local circulatory disturbances, which facilitate secondary infections.
Pathology
Degeneration, necrosis, and shedding of bronchial epithelial cells occur, followed by squamous metaplasia. Cilia become shortened, adhere to one another, tilt, or are lost.
Inflammatory cell infiltration is observed in all levels of the bronchial walls, predominantly neutrophils and lymphocytes. During acute exacerbations, numerous neutrophils may be present, and severe cases may exhibit purulent inflammation.
The mucosa shows congestion and edema, while goblet cells and mucus glands undergo hypertrophy and hyperplasia, leading to excessive mucus secretion and retention.
As the disease progresses, inflammation spreads from the bronchial walls to surrounding tissues. Smooth muscle bundles in the submucosa may rupture and atrophy, while fibrous tissue proliferates in the submucosa and around the bronchi.
Repeated cycles of damage and repair in the bronchial wall lead to structural remodeling, increased collagen deposition, and scar formation.
In advanced stages, when obstructive emphysema develops, alveolar spaces enlarge, and alveolar elastic fibers are destroyed.
Clinical Manifestations
Symptoms
The disease has a slow onset, a long course, and recurrent acute exacerbations that worsen the condition. The main symptoms are cough, expectoration, and wheezing. Acute exacerbations are characterized by a sudden worsening of symptoms such as cough, expectoration, and wheezing. Respiratory infections, caused by viruses, bacteria, mycoplasma, or chlamydia, are the primary triggers of acute exacerbations.
Cough is typically more prominent in the morning, with episodes of nocturnal coughing or sputum expectoration during sleep.
Sputum is usually white, mucoid, or serous and frothy, occasionally streaked with blood. Sputum production is often more abundant in the morning, and positional changes (e.g., getting out of bed) may stimulate expectoration.
Wheezing is more pronounced in patients with coexisting bronchial asthma. In cases complicated by emphysema, exertional dyspnea may occur.
Signs
In the early stages, physical examination may reveal no significant abnormalities.
During acute exacerbations, dry and moist crackles may be heard at the lung bases or posterior chest. These sounds may decrease or disappear after coughing.
In cases of coexisting asthma, widespread wheezing and prolonged expiratory phases may be noted.
Laboratory and Other Auxiliary Examinations
X-ray Examination
Early stages may show no abnormalities. In patients with recurrent episodes, pulmonary markings may appear thickened and disorganized, with reticular, linear, or patchy opacities, more prominent in the lower lungs bilaterally.
Pulmonary Function Tests
Early stages may show no abnormalities. In cases of small airway obstruction, the maximal expiratory flow-volume curve shows significantly reduced flow at 75% and 50% of lung volume. If the ratio of forced expiratory volume in one second (FEV1) to forced vital capacity (FVC) (FEV1/FVC) is less than 70% after using a bronchodilator, it indicates progression to chronic obstructive pulmonary disease (COPD).
Blood Tests
During bacterial infections, there may be an increase in total white blood cell count and/or neutrophil count.
Sputum Examination
Pathogenic bacteria may be cultured from sputum samples. Smears may reveal Gram-positive or Gram-negative bacteria, or large numbers of degenerated white blood cells and goblet cells.
Diagnosis
The diagnosis is based on the presence of cough, expectoration, or wheezing that persists for at least 3 months per year for 2 consecutive years or longer, after excluding other chronic diseases that could cause similar symptoms.
Differential Diagnosis
Bronchial Asthma
Some asthma patients present with irritative cough triggered by dust, fumes, cold air, etc. A history of personal or family allergic diseases is common. Antibiotics are ineffective, and bronchial provocation tests are positive.
Eosinophilic Bronchitis
Symptoms are similar, with no significant changes on X-ray or only increased pulmonary markings. Bronchial provocation tests are often negative. Induced sputum examination showing an increased proportion of eosinophils (≥3%) confirms the diagnosis.
Pulmonary Tuberculosis
It is accompanied by symptoms such as fever, fatigue, diaphoresis, and emaciation. Diagnosis can be confirmed by detecting acid-fast bacilli in sputum and chest X-ray findings.
Lung Cancer
It often occurs in individuals with a long history of smoking. Persistent irritative cough, or a recent change in the nature of a chronic cough, is common. Blood-streaked sputum may also occur. Recurrent obstructive pneumonia in the same location, unresponsive to antibiotics, raises suspicion. Diagnosis can be confirmed through sputum cytology, chest CT, or bronchoscopy.
Idiopathic Pulmonary Fibrosis
It is characterized by a slow clinical course, initially presenting with cough and expectoration, occasionally with tachypnea. Auscultation may reveal crackles (Velcro rales) in the posterior chest. Arterial blood gas analysis shows reduced arterial oxygen partial pressure, while carbon dioxide partial pressure may remain normal. High-resolution spiral CT helps confirm the diagnosis.
Bronchiectasis
Typical symptoms include recurrent cough, production of large amounts of purulent sputum, or hemoptysis. High-resolution spiral CT confirms the diagnosis.
Other Causes of Chronic Cough
These include chronic pharyngitis, upper airway cough syndrome, gastroesophageal reflux, and certain cardiovascular diseases (e.g., mitral stenosis).
Treatment
Treatment During Acute Exacerbations
Empirical antibiotics are often chosen based on the common pathogens in the patient’s region. Oral administration is typical, but intravenous antibiotics may be required for severe cases. Examples include:
- Levofloxacin 0.5 g once daily
- Azithromycin 0.5 g once daily
- Cefuroxime 0.5 g twice daily
If pathogenic bacteria are cultured, antibiotics can be selected based on drug sensitivity testing.
Cough suppression and mucolytics:
- Compound licorice mixture (10 ml, 3 times daily)
- Bromhexine (8-16 mg, 3 times daily)
- Ambroxol hydrochloride (30 mg, 3 times daily)
For patients with predominantly dry cough, antitussive medications can be used.
For patients with wheezing, bronchodilators such as aminophylline (0.1 g, 3 times daily) or sustained-release theophylline can be added, inhaled β2-adrenergic agonists or anticholinergic drugs can also be used.
Treatment During Remission
Treatment options including:
- Smoking cessation and avoidance of harmful gases or particles are essential.
- Strengthening physical fitness and preventing colds.
For patients with recurrent respiratory infections, immunomodulators (e.g., influenza vaccine, pneumococcal vaccine, BCG polysaccharide nucleic acid, thymosin) may be considered.
Prognosis
Some patients can achieve symptom control without significant impact on work or daily life. However, others may progress to chronic obstructive pulmonary disease.