Infantile wheezing bronchitis

　　1. Etiology

　　There are several possible etiological factors, including:

　　1. Infection factors

　　Infections by various viruses and bacteria can cause it. The more common ones include respiratory syncytial virus, adenovirus, rhinovirus, and Mycoplasma pneumoniae, etc. Most cases can develop secondary bacterial infection on the basis of viral infection.

　　2. Anatomical characteristics

　　The trachea and bronchi of infants and young children are relatively narrow, and the surrounding elastic fibers are not well developed, so the mucosa is prone to infection or other stimulation, resulting in swelling and congestion, causing the lumen to narrow, and the secretions to be thick and difficult to be excreted, thus producing wheezing sounds.

　　3. Allergic体质 factors

　　Many infants and young children are infected with viruses, only a small part of whom show symptoms of wheezing bronchitis, indicating that different pathological and physiological changes and clinical manifestations caused by the same virus in different individuals are closely related to intrinsic factors of the body. For example, it has been found that the concentration of histamine in the nasopharyngeal secretions of children with wheezing bronchitis caused by respiratory syncytial virus is significantly higher than that of children with the same infection but without wheezing symptoms. Their relatives often have a history of allergic rhinitis, urticaria, asthma, and other allergic diseases, and about 30% of the children have had eczema, and the serum IgE content is often increased.

　　2. Pathogenesis

　　The pathogenesis of wheezing tracheobronchitis is similar to that of asthma. The pathogenesis of asthma has been studied more in recent years, and it can be roughly divided into the following three aspects.

　　1. Anaphylaxis

　　Is the main cause of the onset of certain asthmatic bronchitis and bronchial asthma. Allergy refers to the reactive changes that occur in the body upon contact with external antigens, which are a special type of immune response. It can be divided into 4 types, namely, immediate hypersensitivity type, cell lysis type, immune complex type, and delayed type. Allergic asthma patients mainly have abnormal type I and type II reactions. The onset of the disease is due to allergic individuals contacting specific antigens, which causes the body to produce reagin antibodies, that is, immunoglobulin E (IgE). Its content in normal serum is very low (0.01～0.09mg), and IgE binds to specific receptors on the membranes of target cells such as mast cells in the bronchial mucosa and submucosa and basophils in the blood, producing sensitization. The tension of the bronchus is mainly regulated by the absolute value and ratio changes of intracellular cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate, with an increase in cAMP stabilizing the mast cells and inhibiting the release of chemical active substances. The Fc segment of the specific IgE molecule can firmly adsorb on the cell surface, while the Fab segment reacts with the antigen (usually two IgE molecules combine with one antigen molecule), activating the enzymatic reaction of the mast cells, causing the calcium channels on the cell membrane to open, calcium ions to enter the cell, and calcium-binding proteins in the cytoplasm, such as calmodulin, to be activated. Subsequently, calmodulin activates phosphodiesterase, thereby promoting the hydrolysis of cAMP. Due to the decrease in cAMP concentration, the stability of the granules in the mast cells is destroyed, leading to degranulation and the release of chemical active substances such as histamine, slow-reacting substances, bradykinin, and eosinophil chemotactic factor (ECF-A). These mediators can stimulate the vagus nerve传入part, causing bronchospasm, histamine can increase the permeability of capillaries and cause tissue edema, slow-reacting substances mainly cause persistent bronchospasm. ECF-A selectively attracts eosinophils to cause allergic tissue damage. Research by the Capital Institute of Pediatrics and other institutions has confirmed that there are specific IgE to mites and蒿属pollen in the serum of children with asthmatic bronchitis and asthma, suggesting that dust mites and蒿属pollen are closely related to the onset of asthmatic bronchitis and asthma. Drug-induced asthma, such as aspirin, can cause asthma, and its pathogenesis is due to aspirin inhibiting cyclooxygenase, thereby inhibiting prostaglandin (PG) synthesis, especially the biosynthesis of PGE. Due to the obstruction of PG synthesis, arachidonic acid can be synthesized into leukotrienes (LT) along the lipoxygenase pathway, mainly LTC4, LTD4, LTE4, which are slow-reacting substances, causing the bronchial smooth muscle to contract strongly and persistently. In addition to IgE, some scholars have found that IgG4, one of the IgG subclasses, can also induce type I hypersensitivity. SIgA is an immune factor for mucosal defense against bacterial and viral invasion, and the Beijing Children's Hospital measured the SIgA in the saliva of asthmatic children, the results were significantly lower than normal, suggesting that the lack or reduction of SIgA is closely related to the onset of asthma. Infants and young children due to poor synthesis ability of SIgA are prone to respiratory tract infections, and external antigens are also easy to enter the body through the respiratory tract, causing an increase in specific IgE in the body.Therefore, the number of people suffering from wheezing bronchitis and asthma has increased. Recently, some people believe that IgG and IgM play a certain role in the onset of asthma. When children inhale allergen, a delayed-type asthma reaction can occur. Gallrame performed lung biopsy on asthma patients, and found the presence of C3 in the pulmonary basement membrane using fluorescence immunotechnology, indicating that complement and immune complexes are involved in the pathogenesis, which is a manifestation of type II hypersensitivity reaction.

　　2. The role of adrenergic receptors

　　Some people believe that all the triggers of asthma pass through a common pathway, that is, the respiratory tract of asthma patients increases its reactivity to various triggers, and smooth muscle spasm can be induced under low-threshold stimulation. The respiratory tract is controlled by the autonomic nervous system. When the vagus nerve is excited, it causes smooth muscle contraction, and the sympathetic nerve causes smooth muscle relaxation. The sympathetic nerve is distributed to the bronchi in a small amount, rather than to the cholinergic ganglia, where it transmits and eliminates the vagus nerve impulse-induced bronchospasm, mainly through the action of catecholamines in the blood circulation and the rich β-receptors. Currently, it is known that at least 4 types of receptors are present in the respiratory tract, namely β-receptors, α-receptors, M-receptors, and H-receptors. These four receptors are all related to respiratory function. When β-receptors and H2-receptors are excited, an increase in intracellular cAMP content leads to bronchial smooth muscle relaxation and antagonizes the effects of other contracting substances. α-receptors and M-receptors bind to the corresponding agonists, respectively, by lowering the level of cAMP and increasing the content of cyclic guanosine monophosphate (cGMP), causing bronchospasm. The HI receptor accepts histamine released by mast cells, causing bronchospasm and edema. Normally, the respiratory tract is mainly β-receptors, and the density of β-receptors on the smooth muscle cells of the trachea to the terminal bronchioles increases progressively, and more than 90% of the β-receptors are β2 subtypes. Therefore, the bronchial smooth muscle mainly relies on the stimulation of β-receptors with β-receptor agonists in the blood circulation to maintain the dilated state of the airways. During asthma, β-receptors often decrease. There are roughly three theories:

　　(1) The theory of reduced responsiveness of β-receptors.

　　(2) The theory of receptor transformation.

　　(3) The theory of β-receptor autoantibodies. It can be seen that the adrenergic receptor is most closely related to asthma.

　　3. Genetic factors

　　As early as 1650, Sennetus reported that in his wife's family, asthma patients appeared in consecutive three generations. William found that 50% of asthma patients had a history of allergic diseases among their close relatives. The survey results of the Department of Pediatrics of Shanghai Medical University show that the incidence rate of asthma in children of all grades of relatives is significantly higher than that of the control group, showing a trend of increase with the proximity of the parents, that is, the closer the parents, the higher the incidence of asthma, indicating that asthma is closely related to heredity. Currently, the international community agrees that asthma is a polygenic hereditary disease, and the genetic laws of the disease are relatively complex. From the analysis of family pedigrees, the following characteristics can be seen:

　　(1) The incidence rate of relatives is often higher than that of the general population, and the closer the kinship, the higher the incidence rate.

　　(2) In a family, the more patients there are, the higher the incidence rate of the relatives, and vice versa.

　　(3) In a family, the higher the severity of the patient's condition, the higher the incidence rate of the relatives, and vice versa.

　　(4) When the incidence of a polygenic hereditary disease has a gender difference in a population, the incidence of relatives of the less common gender patients is actually higher.

　　Generally no complications. It can develop into pneumonia, and some children may later develop asthma. The definition of bronchial asthma is 'Bronchial asthma is a chronic airway inflammation involving various cells and cell components. This inflammation often leads to increased airway reactivity, causing recurrent attacks of wheezing, shortness of breath, chest tightness, and (or) cough, which often occur at night and (or) early morning. These symptoms are often accompanied by widespread and variable airflow obstruction, which can be reversed spontaneously or through treatment.'

　　1. Age

　　The onset age is relatively young, most common in children aged 1 to 3 years.

　　2. General manifestations

　　It often occurs after upper respiratory tract infection, and the condition is usually not severe. There is low or moderate fever, only a few children have high fever, the exhalation time is prolonged, accompanied by wheezing sounds and coarse moist rales, wheezing is not obviously paroxysmal, and the above symptoms are significantly reduced after treatment from the 5th to the 7th day.

　　For children with wheezing bronchitis who have suspected asthma, preventive measures for asthma should be given as soon as possible. Prevention methods for recurrent or chronic bronchitis:

　　1. The general approach is to first find the pathogen, actively treat chronic foci or prevent potential factors to reduce the chance of acute attacks. Secondly, provide reasonable feeding, add complementary foods in a timely manner to enhance physical fitness. Strengthen physical exercise, spend more time outdoors, and, if necessary, take vitamin A orally to increase the resistance of the respiratory tract mucosa.

　　2. The bronchitis vaccine can stimulate the body to produce an immune response, increase the function of phagocytes, and prevent the recurrence of bronchitis. Dosage: Subcutaneous injection once a week during the intercritical period, 0.1ml on the first occasion, and increase by 0.1ml each week if there are no adverse reactions, up to a maximum dose of 0.5ml each time. 10 times make up one course, and effective ones can use several courses, especially starting in the common season, and pausing during the remission period.

　　3. Nucleic acid and casein hydrolysate, known as nucleicase, can enhance the body's resistance. Dosage: Intramuscular injection twice a week, 2ml each time, 10 times as one course. Continue to use if effective.

　　White blood cell count may increase, normal in cases of viral infection, other routine checks show no abnormalities, and eosinophil count. Serum IgE levels may be elevated in some children, chest X-ray examination shows no obvious abnormalities, and there may be changes in bronchitis.

　　1. Choose food according to your daily physical condition.

　　2. Consume more foods rich in vitamins A, C, and calcium.

　　3. Increase the intake of high-protein foods such as lean meat, liver, eggs, poultry, soybeans, and soy products to enhance energy and boost the body's resistance to diseases. People with poor digestion should eat less and more frequently.

　　4. Avoid alcohol and salty food.

　　I. Treatment

　　As an acute bronchitis, appropriate treatment is given.

　　1. General therapy

　　Handle according to the routine of respiratory tract infection, including rest, appropriate indoor temperature and humidity, frequent change of position, more water, and easy-to-digest diet. Pay attention to respiratory isolation to reduce the chance of secondary bacterial infection.

　　2. Infection control

　　The causative agent is mostly viral. Although bacteria are found in the secretion culture, they are not the true causative bacteria, so it is generally not necessary to use broad-spectrum antibiotics. For infants or children with fever or significantly increased white blood cells, appropriate antibiotics can be selected, such as sulfamethoxazole/trimethoprim (Sulfamethoxazole Trimethoprim) oral or penicillin intramuscular injection. If the condition is severe, the age is small, and the constitution is weak, then penicillin and kanamycin (or gentamicin) and other broad-spectrum antibiotics can be used together.

　　3. Symptomatic therapy

　　Including:

　　(1) Cough and sputum removal: The purpose is to make sputum thin and easy to expel. Generally, it is best not to use cough suppressants or sedatives, as they not only suppress the cough reflex and affect the physiological vitality of the cilium, but also make sputum sticky and difficult to expel, causing bronchial obstruction and increasing the chance of bacterial infection. Common expectorants include ipecac syrup 0.1-1ml, three times a day; 10% ammonium chloride 0.1-0.2ml/kg, three times a day; bromhexine (Bisolvon) 2-4mg, three times a day. If dry cough is severe and affects sleep, a small dose of sedative can be given.

　　(2) Asthma cessation: Wheezing is often difficult to control in asthmatic bronchitis. In addition to using bronchodilator drugs such as aminophylline 2-4mg/kg, orally, or using isoproterenol 0.5mg, 4% sodium bicarbonate 2ml for nebulization inhalation. At the same time, pay attention to supplementing water to dilute sputum. In severe wheezing, prednisone (steroid) can be added, 1mg/kg per day, taken three times a day, for 4-7 days as a course of treatment. As for antiallergic drugs such as promethazine (Antihistamine), they can make sputum dry, so they should be used as little as possible.

　　II. Prognosis

　　The prognosis in recent years is generally good, the frequency of recurrence decreases by the age of 3 to 4 years, but some cases may develop into bronchial asthma in the long term.