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Lecture notes, cheat sheets
Hospital pediatrics. Respiratory diseases (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 19. Respiratory diseases. Acute bronchitis. Clinic, diagnosis, treatment, prevention. Chronical bronchitis. Clinic, diagnosis, treatment, prevention 1. Acute bronchitis Acute bronchitis is an acute diffuse inflammation of the tracheobronchial tree. Classification: 1) acute bronchitis (simple); 2) acute obstructive bronchitis; 3) acute bronchiolitis; 4) acute bronchiolitis obliterans; 5) recurrent bronchitis; 6) recurrent obstructive bronchitis; 7) chronic bronchitis; 8) chronic bronchitis with obliteration. Etiology. The disease is caused by viral infections (influenza viruses, parainfluenza viruses, adenoviruses, respiratory syncytial viruses, measles, whooping cough, etc.) and bacterial infections (staphylococci, streptococci, pneumococci, etc.); physical and chemical factors (cold, dry, hot air, nitrogen oxides, sulfur dioxide, etc.). Cooling, chronic focal infection of the nasopharyngeal area and impaired nasal breathing, and chest deformation predispose to the disease. Pathogenesis. The damaging agent enters the trachea and bronchi with inhaled air through the hematogenous and lymphogenous route. Acute inflammation of the bronchial tree is accompanied by a violation of bronchial patency due to an edematous-inflammatory or bronchospastic mechanism. Characterized by hyperemia, swelling of the mucous membrane; on the wall of the bronchus and in its lumen there is a mucous, mucopurulent or purulent secretion; degenerative disorders of the ciliated epithelium develop. In severe forms of acute bronchitis, inflammation is localized not only on the mucous membrane, but also in the deep tissues of the bronchial wall. Clinical signs. Clinical manifestations of bronchitis of infectious etiology begin with rhinitis, nasopharyngitis, moderate intoxication, increased body temperature, weakness, a feeling of weakness, rawness behind the sternum, a dry cough that turns into a wet cough. Auscultatory signs are absent or hard breathing is detected over the lungs, dry rales are heard. There are no changes in peripheral blood. This course is observed more often with damage to the trachea and bronchi. In moderate cases of bronchitis, general malaise, weakness, severe dry cough with difficulty breathing, shortness of breath, and pain in the chest and abdominal wall appear, which is associated with muscle strain when coughing. The cough gradually turns into a wet cough, and the sputum becomes mucopurulent or purulent in nature. In the lungs, upon auscultation, hard breathing, dry and moist fine bubbling rales are heard. Body temperature is subfebrile. There are no pronounced changes in the peripheral blood. A severe course of the disease is observed with predominant damage to the bronchioles. Acute clinical manifestations of the disease begin to subside by the 4th day and, with a favorable outcome, almost completely disappear by the 7th day of the disease. Acute bronchitis with impaired bronchial obstruction has a tendency to protracted course and transition to chronic bronchitis. Acute bronchitis of toxic-chemical etiology is severe. The disease begins with a painful cough, which is accompanied by the release of mucous or bloody sputum, bronchospasm quickly develops (dry wheezing can be heard during auscultation against the background of prolonged exhalation), shortness of breath progresses (up to suffocation), symptoms of respiratory failure and hypoxemia increase. An X-ray examination of the chest organs can determine the symptoms of acute emphysema. Diagnosis: based on clinical and laboratory data. Treatment. Bed rest, plenty of warm drinks with raspberries, honey, linden blossom. Prescribe antiviral and antibacterial therapy, vitamin therapy: ascorbic acid up to 1 g per day, vitamin A 3 mg 3 times a day. You can use cups on the chest, mustard plasters. For a strong dry cough - antitussive drugs: codeine, libexin, etc. For a wet cough - mucolytic drugs: bromine-hexine, ambrobene, etc. Inhalation of expectorants, mucolytics, heated mineral alkaline water, eucalyptus, anise oil using a steam inhaler is indicated Duration inhalations - 5 minutes 3-4 times a day for 3-5 days. Bronchospasm can be stopped by prescribing aminophylline (0,25 g 3 times a day). Antihistamines are indicated, Prevention. Elimination of the etiological factor of acute bronchitis (hypothermia, chronic and focal infection in the respiratory tract, etc.). 2. Chronic bronchitis Chronic bronchitis is a progressive diffuse inflammation of the bronchi, not associated with local or generalized damage to the lungs, manifested by a cough. We can talk about chronic bronchitis if the cough continues for 3 months in the 1st year - 2 years in a row. Etiology. The disease is associated with prolonged irritation of the bronchi by various harmful factors (inhalation of air contaminated with dust, smoke, carbon monoxide, sulfur dioxide, nitrogen oxides and other compounds of a chemical nature) and recurrent respiratory infection (a major role is played by respiratory viruses, Pfeiffer's bacillus, pneumococci), less commonly occurs in cystic fibrosis. Predisposing factors are chronic inflammatory, suppurative processes in the lungs, chronic foci of infection and chronic diseases localized in the upper respiratory tract, decreased reactivity of the body, hereditary factors. Pathogenesis. The main pathogenetic mechanism is hypertrophy and hyperfunction of the bronchial glands with increased mucus secretion, a decrease in serous secretion and a change in the composition of the secretion, as well as an increase in acidic mucopolysaccharides in it, which increases the viscosity of sputum. Under these conditions, the ciliated epithelium does not improve the emptying of the bronchial tree; normally, the entire layer of secretion is renewed (partial cleansing of the bronchi is possible only with a cough). Long-term hyperfunction is characterized by depletion of the mucociliary apparatus of the bronchi, the development of dystrophy and atrophy of the epithelium. When the drainage function of the bronchi is disrupted, a bronchogenic infection occurs, the activity and recurrence of which depend on the local immunity of the bronchi and the occurrence of secondary immunological deficiency. With the development of bronchial obstruction due to hyperplasia of the epithelium of the mucous glands, swelling and inflammatory thickening of the bronchial wall, obstruction of the bronchi, excess viscous bronchial secretions, and bronchospasm are observed. With obstruction of the small bronchi, overstretching of the alveoli during exhalation and disruption of the elastic structures of the alveolar walls and the appearance of hypoventilated or unventilated zones develop, and therefore the blood passing through them is not oxygenated and arterial hypoxemia develops. In response to alveolar hypoxia, spasm of the pulmonary arterioles and an increase in total pulmonary and pulmonary arteriolar resistance develop; pericapillary pulmonary hypertension develops. Chronic hypoxemia leads to an increase in blood viscosity, which is accompanied by metabolic acidosis, which further increases vasoconstriction in the pulmonary circulation. Inflammatory infiltration in large bronchi is superficial, and in medium and small bronchi and bronchioles it is deep with the development of erosions and the formation of meso- and panbronchitis. The remission phase is manifested by a decrease in inflammation and a large decrease in exudation, proliferation of connective tissue and epithelium, especially with ulceration of the mucous membrane. Clinical manifestations. The onset of the disease is gradual. The first and main symptom is a cough in the morning with the discharge of mucous sputum; gradually the cough begins to occur at any time of the day, intensifies in cold weather and becomes constant over the years. The amount of sputum increases, the sputum becomes mucopurulent or purulent. Shortness of breath appears. With purulent bronchitis, purulent sputum may periodically be released, but bronchial obstruction is less pronounced. Obstructive chronic bronchitis is manifested by persistent obstructive disorders. Purulent-obstructive bronchitis is characterized by the release of purulent sputum and obstructive ventilation disorders. Frequent exacerbations during periods of cold, damp weather: cough intensifies, shortness of breath, the amount of sputum increases, malaise and fatigue appear. Body temperature is normal or subfebrile, hard breathing and dry wheezing over the entire pulmonary surface can be detected. Diagnostics. A slight leukocytosis with a rod-nuclear shift in the leukocyte formula is possible. With exacerbation of purulent bronchitis, a slight change in the biochemical parameters of inflammation occurs (C-reactive protein, sialic acids, fibronogen, seromucoid, etc. increase). Sputum examination: macroscopic, cytological, biochemical. With severe exacerbation, the sputum becomes purulent in nature: a large number of neutrophilic leukocytes, an increased content of acidic mucopolysaccharides and DNA fibers, the nature of the sputum, predominantly neutrophilic leukocytes, an increase in the level of acidic mucopolysaccharides and DNA fibers, which increase the viscosity of the sputum, a decrease in the amount of lysozyme, etc. Bronchoscopy, with the help of which endobronchial manifestations of the inflammatory process are assessed, the stages of development of the inflammatory process: catarrhal, purulent, atrophic, hypertrophic, hemorrhagic and its severity, but mainly to the level of the subsegmental bronchi. Differential diagnosis is carried out with chronic pneumonia, bronchial asthma, tuberculosis. Unlike chronic pneumonia, chronic bronchitis always develops from a gradual onset, with widespread bronchial obstruction and often emphysema, respiratory failure and pulmonary hypertension with the development of chronic cor pulmonale. On X-ray examination, the changes are also diffuse in nature: peribronchial sclerosis, increased transparency of the pulmonary fields due to emphysema, expansion of the branches of the pulmonary artery. Chronic bronchitis differs from bronchial asthma in the absence of asthma attacks; it is associated with pulmonary tuberculosis by the presence or absence of symptoms of tuberculosis intoxication, Mycobacterium tuberculosis in sputum, the results of X-ray and bronchoscopic examination, and tuberculin tests. Treatment. In the phase of exacerbation of chronic bronchitis, therapy is aimed at eliminating the inflammatory process, improving bronchial patency, as well as restoring impaired general and local immunological reactivity. Antibiotic therapy is prescribed, which is selected taking into account the sensitivity of the sputum microflora, administered orally or parenterally, and sometimes combined with intratracheal administration. Inhalations are indicated. Use expectorants, mucolytic and bronchospasmolytic drugs, and drink plenty of fluids to restore and improve bronchial patency. Herbal medicine using marshmallow root, coltsfoot leaves, and plantain. Proteolytic enzymes (trypsin, chymotrypsin) are prescribed, which reduce the viscosity of sputum, but are currently rarely used. Acetylcysteine has the ability to break disulfide bonds of mucus proteins and promotes strong and rapid liquefaction of sputum. Bronchial drainage is improved with the use of mucoregulators that affect secretions and the production of glycoproteins in the bronchial epithelium (bromhexine). In case of insufficient bronchial drainage and existing symptoms of bronchial obstruction, bronchospasmolytics are added to treatment: aminophylline, anticholinergic blockers (atropine in aerosols), adrenergic stimulants (ephedrine, salbutamol, Berotec). In a hospital setting, intratracheal lavages for purulent bronchitis must be combined with sanitation bronchoscopy (3-4 sanitation bronchoscopy with a break of 3-7 days). When restoring the drainage function of the bronchi, physical therapy, chest massage, and physiotherapy are also used. When allergic syndromes develop, calcium chloride and antihistamines are used; if there is no effect, a short course of glucocorticoids can be prescribed to relieve allergic syndrome, but the daily dose should not be more than 30 mg. The danger of activation of infectious agents does not allow long-term use of glucocorticoids. In patients with chronic bronchitis, complicated respiratory failure and chronic cor pulmonale, the use of veroshpiron (up to 150-200 mg/day) is indicated. The food of patients should be high-calorie and fortified. Use ascorbic acid 1 g per day, nicotinic acid, B vitamins; if necessary, aloe, methyluracil. With the development of complications of a disease such as pulmonary and pulmonary-heart failure, oxygen therapy and auxiliary artificial ventilation are used. Anti-relapse and maintenance therapy is prescribed in the subsiding phase of exacerbation, carried out in local and climatic sanatoriums, this therapy is prescribed during clinical examination. It is recommended to distinguish 3 groups of clinical patients. 1st group. It includes patients with cor pulmonale, severe respiratory failure and other complications, and loss of ability to work. Patients are prescribed maintenance therapy, which is carried out in a hospital or by a local doctor. These patients are examined at least once a month. 2nd group. It includes patients with frequent exacerbations of chronic bronchitis, as well as moderate dysfunction of the respiratory system. Such patients are examined by a pulmonologist 3-4 times a year, and anti-relapse therapy is prescribed in the fall and spring, as well as for acute respiratory diseases. An effective method of administering drugs is the inhalation route; according to indications, it is necessary to carry out sanitation of the bronchial tree using intratracheal lavages, sanitation bronchoscopy. In case of active infection, antibacterial drugs are prescribed. 3rd group. It includes patients in whom anti-relapse therapy led to a subsidence of the process and the absence of relapses for 2 years. Such patients are indicated for preventive therapy, which includes means aimed at improving bronchial drainage and increasing its reactivity. Author: Pavlova N.V. << Back: Congenital and hereditary lung diseases (Agenesis, aplasia and hypoplasia of the lungs. Polycystic lung disease. Congenital lobar emphysema. Williams-Campbell syndrome. Tracheobronchomegaly. Mounier-Kuhn syndrome. Primary ciliary dyskinesia (fixed cilia syndrome) and Kartagener syndrome. Idiopathic diffuse pulmonary fibrosis (Hammen-Rich syndrome, idiopathic fibrosing alveolitis - ELISA). Primary pulmonary hypertension (AERSA syndrome). Idiopathic pulmonary hemosiderosis (Zelen-Gellerstedt syndrome). Goodpasture syndrome. Connective tissue pathology. Alveolar microlithiasis. Alveolar proteinosis. Lung lesions due to deficiency of a - protease inhibitor. Cystic fibrosis)
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