Chronic bronchitis is a chronic nonspecific inflammation of the tracheobronchial mucosa and peripheral tissues, and is characterized clinically by cough, expectoration, with or without wheezing, and duration greater than 3 months every year for at least 2 consecutive years.

Etiology and pathogenesis

The etiology of this disease is not fully understood, and may be the result of long-term interaction between multiple environmental factors and the body's own factors.

Cigarette smoking is the most important environmental factor. The prevalence of chronic bronchitis in smokers is 2 - 8 times more common than in non-smokers. The risk of disease occurrence is directly proportional to smoking pack years. Chemical substances such as tar, nicotine, and hydrocyanic acid in tobacco have multiple damaging effects, which can damage airway epithelial cells and ciliary movement, reducing airway purification ability; cause hyperplasia and hypertrophy of bronchial mucous glands and goblet cells, increasing mucus secretion; stimulate parasympathetic nerves, contracting bronchial smooth muscles and increasing airway resistance; and increase the production of oxygen free radicals, inducing neutrophils to release proteases, destroying pulmonary elastic fibers, and inducing the formation of emphysema.

Long-term exposure to high concentrations of occupational dust, environmental dust, and harmful particles such as fumes and allergens may contribute to chronic bronchitis.

Various harmful gases, such as sulfur dioxide, nitrogen dioxide, and chlorine, and PM2.5 can damage the airway mucosal epithelium, which leads to reduction of the ciliary clearance function and increase of mucus secretion, thereby creating conditions for bacterial infection.

Infection with viruses, mycoplasma, and bacteria is an important cause of the occurrence and development of chronic bronchitis. Common viruses are influenza virus, rhinovirus, adenovirus, and respiratory syncytial virus, as well as coronavirus. Bacterial infection is often secondary to viral infection, and common pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus. These infectious factors also contribute to damage and chronic inflammation of the tracheobronchial mucosa.

Body factors such as immunodeficiency, airway hyperresponsiveness, autonomic dysfunction, and aging; and environmental factors such as climate are associated with the occurrence and development of chronic bronchitis. For example, due to the impaired adrenal cortex function, decreased cellular immunity, and reduced lysozyme activity, older adults are more susceptible to respiratory infection. Cold air can stimulate the glands to increase mucus secretion, weaken ciliary movement, contract mucosal blood vessels, and cause local blood circulation disorders, which is conducive to secondary infection.

Pathology

Bronchial epithelial degeneration, necrosis, and exfoliation are followed by squamous metaplasia and shortened, adhesive, lodged, and lost cilia. The bronchial walls are with inflammatory cell infiltration, mainly neutrophils and lymphocytes. In the acute stage, numerous neutrophils, suppurative inflammation in severe patients, mucosal congestion and edema, hypertrophy and hyperplasia of goblet cells and mucous glands, and mucous retention can be observed. With the progression of the disease, the inflammation spreads from the bronchial wall to the peripheral tissues, the submucosal smooth muscle bundles may be fractured and atrophied, and the submucosal and peribronchial fibrous hyperplasia occurs. The damage-repair process of the bronchial walls occurs repeatedly, resulting in bronchial structural remodeling, increased collagen content, and scar formation. When it develops into obstructive emphysema, the alveolar cavities are enlarged and the alveolar elastic fibers are fractured.

Clinical manifestations

Slow onset, long duration, and recurrent acute attacks aggravate the symptoms. The main symptoms are cough and expectoration, with or without wheezing. Acute exacerbation mainly results from respiratory infection, and the pathogens can be viruses, bacteria, mycoplasma, and chlamydia.

Cough occurs mainly in the morning, and paroxysmal cough or expectoration may occur during sleep. Sputum is generally white mucus or serous foam, occasionally bloody. Wheezing may be accompanied by bronchial asthma. If accompanied by emphysema, tachypnea after exercises is present.

There are usually no abnormal signs in the early stage. During the acute attacks, dry and moist crackles can be heard on the back or at the bottom of both lungs, and may reduce and subside after cough. If accompanied by asthma, extensive wheezing and prolonged expiratory periods are present.

Laboratory and auxiliary examinations

X-ray

There may be no abnormalities in the early stage. In patients with recurrent episodes, thickened, disordered lung markings, with reticular, linear, or mottled opacities, are apparent in the lower lungs.

Respiratory function examination

There are no abnormalities in the early stage. In the presence of small airway obstruction, the maximal expiratory flow-volume curve shows a significant reduction in flow at 75% and 50% of lung capacity. The ratio of forced expiratory volume in one second (FEV₁) to forced vital capacity (FVC) after inhalation of bronchodilators (FEV₁/FVC) < 0.70 suggests chronic obstructive pulmonary disease.

Blood test

In the case of bacterial infection, total white blood cell count or neutrophil count or both may be elevated.

Sputum examination

Pathogenic bacteria can be cultured. Smears can reveal Gram-positive or Gram-negative bacteria, or numerous destroyed white blood cells and goblet cells.

Diagnosis

On the basis of cough and expectoration, with or without wheezing, duration greater than 3 months each year for at least 2 consecutive years, and exclusion of other chronic diseases that can cause similar symptoms, a clinical diagnosis can be established.

Differential diagnosis

Bronchial asthma

Asthma is characterized by irritable cough in some patients. Dust, oil fume, and cold air can easily induce cough. Patients often have a familial or personal history of allergic diseases. Antibiotics are ineffective, and bronchial provocation test is positive.

Eosinophilic bronchitis

The clinical symptoms resemble those of chronic bronchitis. Chest x-ray shows inapparent changes or increased lung markings. Bronchial provocation test is predominantly negative. Clinical misdiagnosis can occur easily. Diagnosis is established on the basis of an increase in the proportion of eosinophils (>3%) in induced sputum examination.

Pulmonary tuberculosis

It often presents with fever, fatigue, diaphoresis, and emaciation. Acid-fast bacilli isolated from sputum and chest x-ray can assist in the identification.

Bronchogenic carcinoma

Most patients have a history of cigarette smoking, refractory and irritable cough, or a history of cough. Cough is often with bloody sputum recently. Sometimes, it presents with recurrent obstructive pneumonia in the same site that does not completely resolve after antibiotic treatment. Exfoliative cytology, chest CT, and bronchoscopy can be used to confirm the diagnosis.

Idiopathic pulmonary fibrosis

It presents with a slow clinical process and cough, expectoration, and occasionally tachypnea in the early stage. Crackles (Velcro crackles) on the lower posterior chest can be heard on auscultation. Blood gas analysis shows a decrease in the arterial partial pressure of oxygen, but no increase in the partial pressure of carbon dioxide. High-resolution spiral CT can assist in the diagnosis.

Bronchiectasis

The typical manifestations are recurrent cough, purulent expectoration, and hemoptysis. High-resolution spiral CT can assist in the definitive diagnosis.

Other diseases that cause chronic cough

Other diseases that cause chronic cough include chronic pharyngitis, upper airway cough syndrome, gastroesophageal reflux, and certain cardiovascular diseases such as mitral stenosis.

Treatment

Antibiotics are often selected based on the empirical common pathogens, generally oral, but intravenous in severe patients. The treatment plan is levofloxacin 0.4g once a day, azithromycin 0.5g once a day, or cefuroxime 0.5g twice a day. If the pathogen can be cultured, the most effective antibiotics can be chosen based on the antibiotic sensitivity test.

Antitussives and expectorants can be administered, and the treatment regimen is bromhexine 8 - 16mg 3 times a day or ambroxol hydrochloride 30mg 3 times a day. Patients with dry cough can be treated using antitussives.

Patients with wheezing can be treated using bronchodilators such as aminophylline and theophylline extended-release tablets, inhaled β₂ receptor agonists, and anticholinergics.

Prognosis

The disease can be under control in most patients, and does not affect their work and study. However, it can also progress into chronic obstructive pulmonary disease in some patients.