Irreversible damage to the tracheal wall due to congenital or acquired factors causing bronchial dilatation and luminal obstruction, often associated with bronchiectasis and pulmonary cystic fibrosis. It is classified as an obstructive lung disease. The disease was first discovered in 1819, and he was also the inventor of the stethoscope. The theory of bronchiectasis was further refined in the 1800s by the famous Canadian physician Osler, who was also later thought (and not diagnosed) to have died from complications of bronchiectasis.
Bronchiectasis may involve multiple regions of the lung, called diffuse, or only one or two regions, called restrictive. Typical bronchial dilatation causes damage to only moderate caliber bronchi, but scarring and destruction of even smaller bronchi is often seen.
I. Pathogenesis.
Direct damage to the bronchial wall or indirect damage due to disruption of the normal defense mechanisms of the respiratory tract can lead to bronchiectasis.
The defense mechanism of the respiratory tract includes the cellular cilia on the surface of the respiratory tract, which constantly move back and forth to expel the thin mucus (sputum) that is covered on the surface of the respiratory tract, and also to expel the harmful particles and bacteria deposited in the respiratory mucus from the body. Regardless of direct or indirect damage to the respiratory tract, chronic inflammation of the bronchial wall occurs, causing loss of elasticity of the bronchi, resulting in dilatation, relaxation and expansion of the respiratory tract in the form of a thin-walled sac; inflammation also increases mucus secretion; due to the destruction of ciliated cells, this mucus collects in the dilated respiratory tract, nourishing the reproduction of bacteria. Bacteria further damage the tracheal wall, leading to a vicious circle of infection and bronchial damage.
In summary, bronchial dilatation is irreversible because of: increased mucus secretion (sputum), destruction of cilia of cells, and destruction of bronchial walls due to chronic inflammation.
II. Etiology.
There are two types of etiologies, congenital and acquired.
1. Congenital causes: The following hereditary diseases can cause bronchiectasis, primary ciliary dyskinesia, which causes ciliary dyskinesia in the bronchial wall, resulting in bronchiectasis. A small percentage of patients with cystic fibrosis of the lungs can develop severe bronchiectasis. young syndrome, with clinical manifestations similar to cystic fibrosis, has conditions including: bronchiectasis, sinusitis and low fertility (sperm deficiency), which is associated with obstruction of the bronchi and vas deferens containing large amounts of mucous secretions. Patients with alpha-antitrypsin deficiency are also highly susceptible to bronchiectasis for unknown reasons. Other rare congenital causes include: primary immunodeficiency; bronchiectasis can sometimes be combined with inflammatory bowel disease, especially ulcerative colitis, and occasionally Crohn’s disease.
2. The most common cause is acquired: severe or recurrent respiratory infections, of which endobronchial tuberculosis has the highest incidence. Other etiologies include: immune deficiency, mechanical factors (e.g., airway obstruction due to respiratory tumors or inhalation of foreign bodies, inhalation of toxic fumes, smoking, inhalation of silica, coal dust, and other harmful particles).
3, another occasional disease involving the atmospheric tract, namely: allergic bronchopulmonary aspergillosis, which often occurs in asthmatic patients, its a metabolic disease to Aspergillus, which can cause sputum clots to obstruct the airways and lead to bronchodilation. Recent studies have shown that patients with rheumatoid arthritis who smoke are at high risk for bronchiectasis.
Third, bronchiectasis typing.
Depending on the severity of the lesion, bronchiectasis is divided into three types: fusiform (cylindrical) bronchiectasis, the most common, which is a mildly inflamed bronchus causing destruction of the normal bronchial morphology of the distal tapering; varicose bronchiectasis, in which the bronchial wall is beaded, which is due to the morphology of mixing the dilated and narrowed parts of the bronchus; cystic bronchiectasis, characterized by severe, irreversible peripheral bronchus in the shape of a balloon, which can be be accompanied by or without gas-fluid flattening.
IV. Symptoms.
1. Bronchiectasis can occur at any age, with primary symptoms often appearing in early childhood or adolescence, but patients are mostly diagnosed after the age of 20. Symptoms show gradual aggravation after lung infection and last for years. The most typical symptoms are chronic cough, coughing sputum, hemoptysis, recurrent fever and chest pain with or without pneumonia, wasting, and anemia.
2. Most patients present with chronic cough, coughing sputum, which may be white or yellow-green in color and may be accompanied by foul odor or blood, which is obvious when changing position (e.g. lying in bed, turning on one’s side, etc.).
3. The amount of coughing sputum is related to the extent of lesion involvement and whether it is complicated by infection, usually heavy in the morning and light in the evening, and is often accompanied by hemoptysis due to brittle, multi-vascularized bronchial wall damage, and hemoptysis may be the first symptom, or even the only symptom, which is fatal.
4.Patients with extensive bronchiectasis may experience wheezing or shortness of breath. Patients who have developed pulmonary heart disease or respiratory failure may also experience easy fatigue, lethargy, and dyspnea, and these symptoms are more pronounced after activity.
5, long-term coughing pus sputum patients with bronchial dilatation will cough up sputum every day. Patients with bronchiectasis are easily infected with Haemophilus influenzae in the initial stage, while secondary infections are usually Staphylococcus aureus, followed by Moraxella mucosae, and finally Pseudomonas aeruginosa infection.
V. Complications.
Recurrent infections and inflammatory reactions in the small airways in the lungs can lead to pneumonia, scar formation and pulmonary decompensation. Severe pulmonary scarring and pulmonary decompensation eventually lead to right heart failure, known as pulmonary heart disease. Very severe branched dilatation forming progressive cystic fibrosis of the lung is mostly seen in underdeveloped countries or regions, and its impairment of lung function can lead to decreased blood oxygen levels and increased carbon dioxide levels, which is known as respiratory failure.
VI. Diagnosis.
The doctor will consider the diagnosis of bronchiectasis based on the patient’s present or past symptoms and manifestations. Abnormal breath sounds can often be heard on auscultation, and the doctor will also perform targeted tests to clarify the diagnosis and assess the extent and location of the lesion.
Chest X-ray is the most commonly used test, but occasionally the chest X-ray is normal. At present, high-resolution CT of the chest has replaced the traditional bronchial iodine-oil imaging as the gold standard for the diagnosis of bronchiectasis, which can clarify the diagnosis and determine the location, extent and scope of the lesion.
After the diagnosis of bronchiectasis, a number of tests will be done to investigate the cause of bronchiectasis, these tests include
1. measuring the level of a certain protein in the blood.
2. checking for HIV infection or other immune dysfunctional diseases
3. determination of the salt content of sweat, which is abnormal in patients with cystic fibrosis
4. nasal and bronchial or sputum smears and bacterial cultures.
5. bronchoscopy to exclude inhaled bronchial foreign bodies or tumours if the bronchial dilatation is confined to only one area, such as within one lobe of the lung or one lung segment
6. other tests for structural and functional damage to mucosal cilia
7. examinations to exclude tuberculosis, certain fungal infections, tumors, etc.
8.Allergic bronchopulmonary aspergillosis.
Genetic determination is required to exclude pulmonary cystic fibrosis in patients with a family history of recurrent respiratory infections in young children who present with cystic fibrosis.
VII. Prevention
Early diagnosis and treatment of diseases that predispose to bronchiectasis can prevent its development or reduce its severity. More than half of the patients with bronchiectasis are diagnosed accurately and treated aggressively in childhood. It is important to note, however, that some patients with bronchiectasis are not preventable. Improving the quality of life and good nutritional status can undoubtedly significantly reduce the incidence of bronchiectasis, so a scientific view of diet (see the article on diet for tumor prevention on this site) and maintaining a normal body mass index should be established.
1. Vaccination: Vaccination against measles, rubella and pertussis during childhood, and annual vaccination against influenza and pneumococcal vaccine. Chest X-ray should be taken immediately after a child has severe measles, whooping cough or other lung infections.
2. Early treatment: Appropriate antimicrobial agents (i.e., not to be abused or not to be used) applied early in the early stages of lung infection can help prevent bronchial expansion and reduce the severity of its attacks.
3, treatment of the original disease: with allergic bronchopulmonary aspergillosis, the appropriate application of hormones and antifungal drugs can reduce bronchial damage and prevent bronchial expansion. For people with immunoglobulin deficiency syndrome, receiving immunoglobulin injection can prevent recurrent infections.
4, respiratory protection: avoid inhalation of toxic fumes, harmful dust, avoid smoking, etc., can prevent bronchiectasis and reduce its attacks. Although there is no evidence that smoking can cause bronchiectasis, it is clear that smoking can irritate the patient’s bronchial tubes and aggravate infections and other complications. Use hand sanitizer with antibacterial effect to wash hands appropriately.
5. Avoid inadvertent inhalation in the trachea: children should be prevented from holding hard objects in their mouths in time to avoid inadvertent inhalation into the trachea causing secondary bronchiectasis. Avoid taking excessive sedatives, intoxicating alcohol and neurological drugs that cause loss of consciousness or gastrointestinal reactions. Also, do not inject Vaseline or mineral oil into the nasal cavity to prevent inadvertent aspiration into the lungs that cannot be expelled.