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Lung diseases are the main symptoms. Congenital malformations of the lungs in children Lung diseases symptoms and treatment

Lung malformation are serious changes in the structure of the lungs that occur in the embryo at the initial stage of the formation and development of the bronchopulmonary system. These changes can cause significant dysfunction of the respiratory system. At an early age, lung malformations may be accompanied by respiratory failure, which leads to a delay in the child’s physical development.

The occurrence of defects can occur under the influence of external factors affecting the embryo. These include various injuries, poisoning with chemical poisons, and viral infections that occur during the first trimester of pregnancy. There are also internal reasons for the formation of defects - these are heredity, inferiority of germ cells during late pregnancy, abnormalities of genes and chromosomes.

Types and their description

There are several groups of lung malformations, united by common characteristics.

First group combines defects characterized by underdevelopment of the lung or its elements. In these cases, the lung and main bronchus are either completely absent (agenesis), or in the absence of the lung, part of Bericht's bronchus is present (aplasia). These defects are extremely rare. In the absence of one lung, children are born quite viable; with bilateral agenesis or aplasia, they die. Sometimes there is simultaneous underdevelopment of the lung and bronchi (hypoplasia), in which the lungs are reduced in size, but have the correct structure and are able to perform the necessary functions.

Second group includes malformations of the walls of the trachea (windpipe) and bronchi. There are cases of dilatation of the trachea and bronchi, resulting from poor development of the elastic muscle fibers of their walls (tracheobronchomegaly), softening of the cartilage of the trachea and bronchi (tracheobronchomalacia). The presence of such congenital defects is subsequently expressed by frequent diseases of tracheobronchitis, rough cough, and difficulty breathing. Symptoms in the form of shortness of breath, attacks of suffocation, coughing up blood can be a consequence of a defect associated with underdevelopment or complete absence of the cartilaginous and elastic tissues of the bronchi (Williams-Campbell syndrome).

This group also includes a congenital lung defect, in which an increased volume of oxygen accumulates in the lungs due to their excessive expansion. Externally it manifests itself as a barrel-shaped enlargement in the chest area, accompanied by respiratory failure. There is a defect characterized by a sharp narrowing of the bronchi habe and trachea (stenosis), this is a consequence of insufficient development of cartilage rings or compression of blood vessels. This defect leads to impaired swallowing function. Particular problems with cheap nba jerseys eating arise when a defect is formed, in which an open connection occurs between the esophagus and trachea (fistula), food can enter the respiratory tract, and attacks of suffocation occur during feeding. Sometimes during the examination a defect is revealed, which is characterized by weakness or underdevelopment of the muscle frame and elastic tissue of the bronchi (diverticula).

To the third group These include defects for which excessive formations in the lung area are typical. One of them is a cystic adenomatous lung defect, characterized by the final proliferation of small branches of the New bronchi (bronchioles), while the vessels into which air penetrates (alveoli) are not affected. Growing formations (cysts) can vary in size. This defect can cause a shift in the position of the heart, which subsequently leads to polyhydramnios (non-immune hydrocele). Sometimes additional formations of lung tissue are found, despite the presence of an already formed organ (additional lobe), a section independently developing from the lung (sequestration), small formations in the form of tumors, consisting, in addition to lung tissue, of elements of the walls of the bronchi (hamartoma). Very often, these formations are detected by chance during examination for other lung diseases.

Fourth group combines defects associated with abnormal arrangement of organs. A defect typical of many internal organs is the reverse arrangement (Kartagener's syndrome). Its presence is accompanied by chronic bronchitis.

Fifth group includes malformations of blood vessels. These include stenosis (narrowing of blood vessels), which occurs mainly with heart defects; defects in which communication channels wholesale mlb jerseys are formed between the beds of veins and arteries (aneurysms); insufficient development of branches of the pulmonary artery.

Treatment methods and prevention

The presence of congenital lung defects requires treatment in the form of traditional therapy measures; they are taken to prevent the occurrence of purulent cheap nfl jerseys processes. Annual courses of anti-inflammatory therapy are required, which include procedures for washing (sanitizing) the bronchi, taking drugs with an expectorant effect, inhalations, physical therapy, and massages. Rehabilitation in special sanatoriums is recommended.

The decision to undergo surgery is made by the doctor. Surgery may be prescribed for severe respiratory dysfunction due to existing defects.

Prevention involves avoiding adverse effects during pregnancy, counseling and examination by health professionals. If a lung defect is detected in the fetus, observation becomes intensified.

Covers a spectrum of cystic and adenomatous formations in the lobes, which are hamartomas with a cystic structure.

Exclude concomitant organ defects (up to 20%): kidneys, small intestine, diaphragmatic hernia, hydrocephalus, skeletal anomalies.

Prenatal diagnosis: polyhydramnios (compression of the esophagus or direct communication of the cyst with the respiratory tract) or dropsy (heart failure due to impaired venous return).

Diagnosis: Chest x-ray - multiple discrete blisters are visible, often with fluid levels within a single lobe.

First aid: consultation with a surgeon, planning the operation. With a prenatal diagnosis - as early as possible.

Beware pulmonary hypertension of a healthy lung.

Congenital lobar emphysema

Congenital lobar emphysema: almost always an emergency condition with overinflation of one lobe of the lung (without emphysematous destruction of lung tissue).

Causes: malformations of cartilage, bronchial tree, stenosis or external compression (vascular abnormality or tumor), polyalveolar lobe.

Caution: Always rule out mucus (meconium) plug as the cause (bronchoscopy).

Complications/problems: displacement, compression and excess blood flow in healthy lung tissue.

First aid: observation → surgery. Emergency surgery (lobectomy) is rarely required.

Lung sequestration

Lung sequestration: cystic or homogeneous area, in most cases in the lower lobes, usually on the left. This is a non-functional tissue not associated with the bronchial system. The blood supply comes most often from the aorta. Venous drainage can be into the systemic or pulmonary veins. They develop from an accessory lung bud from the foregut. The earlier the defect is formed, the more often the lung and sequestrum have a common pleura.

Increased likelihood of associated defects.

Complications: enlarged left-to-right shunt and, as a result, heart failure (> 80% of anastomoses with vessels of the esophagus or fundus of the stomach).

Prenatal diagnosis: Ultrasound.

Diagnostics, after birth, X-ray, if necessary, CT, angiography (MRI angiography) and scantigraphy with methylene diphosphonate (accumulation in the sequestrum).

Treatment: the method of choice is surgery, even in the absence of a clinic due to the risk of infection. Before surgery - treatment according to the clinical picture.

Agenesis and aplasia of the lungs

Bilateral agenesis is an extremely rare defect that is incompatible with life. Sometimes the trachea is also missing. Bronchial arteries and veins are usually absent. May be combined with defects of the esophagus, face and asplenia. A unilateral process is much more common; in 50-60% of patients, other congenital defects are observed: of the heart, genitourinary system, vertebrae and ribs, diaphragmatic hernia, etc. The only lung is compensatory enlarged. Bronchiectasis is often found in it.

Pulmonary hypoplasia (small lung)

Pulmonary hypoplasia occurs in 10% of childhood autopsies and in 85% of cases is combined with other congenital defects. Clinically characterized by the development of SDR, the severity of which depends on the degree of hypoplasia. Congenital pulmonary hypoplasia can be primary, or idiopathic, and secondary (much more often), unilateral and bilateral. Primary pulmonary hypoplasia is caused by genetic factors. It has been described in trisomies 13, 18 and 21, some genetic syndromes, in twins, and family cases are known.

Causes of secondary hypoplasia:

  1. abnormalities of the vessels supplying the lung (pulmonary stenosis, tetralogy of Fallot, etc.);
  2. oligohydramnios;
  3. compression of the lungs by intrathoracic masses (congenital diaphragmatic hernia, congenital hydrops fetalis);
  4. compression of the lungs due to chest deformities (asphyxial thoracic dystrophy, severe scoliosis);
  5. lack of respiratory movements in the uterus due to neuromuscular diseases.

The diagnosis of idiopathic pulmonary hypoplasia is made in the absence of all the above reasons. The pathological anatomy of both forms of hypoplasia is the same. Macroscopically: both lungs may be uniformly reduced, or there is pronounced asymmetry (for example, with a diaphragmatic hernia). In cases where hypoplasia is the direct cause of death, lung weight is reduced by more than 40% and is often only 20-30% of normal weight for gestational age. Normally, full-term fetuses and newborns have a lung weight of -50 g. The indicator of relative lung weight is of greater importance for determining hypoplasia, i.e. ratio of lung weight to fetal weight. Normally, in fetuses and newborns 28 weeks of pregnancy and older, this figure is 0.012, in premature infants up to 28 weeks - 0.015 (interpreting the indicator of relative lung mass, it is necessary to take into account that in the presence of pathological processes in the lungs, such as pneumonia, HD, aspiration syndromes, etc., the relative weight will be higher). Depending on the microscopic picture, two main forms of pulmonary hypoplasia are distinguished. In the first case, the lungs are small, but in terms of maturity they correspond to gestational age, although the number of alveoli is reduced; in the second case, pronounced immaturity of the lung tissue is observed. This form is combined with oligohydramnios. Special staining reveals the absence of elastic tissue in the interlobar septa. Immunohistochemically, a significant decrease in the amount of type IV collagen is determined. Morphometric studies show that, regardless of the cause, the alveolar radial count is reduced in the hypoplastic lung. Alveolar radial count is easily determined on histological preparations by the number of alveolar septa located on a straight line drawn perpendicularly from the terminal bronchiole to the pleura or lobular septum. In full-term infants, the normal radial alveolar count is 4.1-5.3. Another method for determining hypoplasia is to measure the amount of lung DNA as an indicator of the total cell population of the lungs.

Pulmonary hyperplasia

More often it is a secondary defect. Lung enlargement is observed in cystic-adenomatous lung defects, congenital emphysema, as a compensatory process for unilateral agenesis or hypoplasia. True hyperplasia is always a bilateral process caused by obstruction in the upper respiratory tract. Lung hyperplasia in combination with laryngeal atresia is observed in autosomal recessive Fraser syndrome, characterized by cryptophthalmos, abnormalities of the ears, kidneys, syndactyly and cryptorchidism. Macroscopically: with a pronounced increase in the lungs, the diaphragm is shifted downwards, the lungs have imprints of the ribs, the relative weight is increased. Microscopically: more mature lung tissue with an increase in alveolar surface compared to the weight of the newborn and the gestational age. Hyperplasia of the lung with laryngeal atresia is caused by the lack of outflow of fluid from the lungs into the amnion cavity due to obstruction.

Accessory lung (tracheal accessory lung)

This extremely rare defect is caused by a violation of the division of the primary bronchial kidneys. It is necessary to differentiate with pulmonary sequestration and with “tracheal bronchus”.

Horseshoe lung

Refers to rare defects in which the lungs are partially connected by their bases behind the heart and in front of the esophagus. In the absence of other defects, it is asymptomatic, but it has been described in combination with various vascular anomalies of the lungs and other defects, such as hypoplasia of the right or left lung and scimitar syndrome.

Ectopic pulmonary tissue

There may be ectopic pulmonary tissue in the neck, abdominal cavity and chest wall, often combined with skeletal abnormalities and diaphragmatic hernia. Sometimes ectopic lung tissue in the abdominal cavity is referred to as extralobar sequestration. Neck ectopia is observed with inioncephaly, Klippel-Feil anomaly and cry-the-cat syndrome. The causes of pulmonary ectopia are not known.

Heterotopias in the lungs

Heterotopias have been described in the form of islands of tissue of the adrenal glands, pancreas, thyroid gland (without C-cells), liver, striated muscles, which are also found in pulmonary sequestra and hypoplastic lung. Their significance is small, since such heterotopias are observed only in children with other severe defects, mainly of the heart. In case of anencephaly, foci of glial tissue may enter the lung through the bloodstream or during ingestion. As a result of birth trauma, emboli from cerebellar tissue can be observed in the vessels, which are sometimes mistaken for hamartomas or heterotopic tissue.

Cystic lung disease

The existing classification of cystic lung disease is far from ideal. Currently, a distinction is made between congenital and acquired cysts. Acquired cysts in infants can be a consequence of infection, compression of the bronchus by an enlarged pulmonary artery, the presence of a foreign body in the bronchus, or bronchial hypoplasia. We do not consider them in this section. Congenital cysts include: bronchogenic cysts, pulmonary sequestration, cystic adenomatous lung disease, polyalveolar lobe, congenital lobar emphysema, lymphangiomatous cysts and enterogenic cysts.

Congenital lung cysts.

Rare vice

Cysts are single or multiple, always associated with the bronchial tree (postnatally often filled with fluid), limited to one lobe.

Differential diagnosis: pneumothorax.

Treatment: surgery is the method of choice. For tense cysts, they can be punctured as an emergency measure. Increase in size and tension can occur very quickly.

Bronchogenic cysts- These are congenital cystic formations. caused by impaired development of the primary intestine. They are usually located in the mediastinum near the carina of the trachea (51%), but can be located in the right paratracheal region, along the esophagus, at the hilum of the lung, or in various other locations. Bronchogenic cysts are rarely connected to the tracheobronchial tree or located in the lung tissue. In newborns they are asymptomatic or can cause SDR. Macroscopically: a round cyst with a smooth or rough internal surface, 1-4 cm in diameter, attached to the tracheobronchial tree, but not connected to it. The contents are a clear serous fluid, in cases of infection it is cloudy or bloody. Microscopically: the cyst is lined with ciliated cubic or columnar epithelium, sometimes squamous metaplasia is observed. The wall consists of a small amount of connective tissue, smooth muscle, pockets of cartilage and rarely bronchial glands. Bronchogenic cysts are combined with pulmonary sequestration, an additional lobe of the lung, described in Down syndrome.

Extralobar sequestration diagnosed in infants under 1 month of age. The ratio of boys: girls is 4: 1. Macroscopically: an isolated area of ​​the lung with its own pleura, often cystically changed. It is located anywhere - from the neck to the diaphragm, most often behind the left lower lobe, and a diaphragm defect is often detected. May be located deep in the diaphragm or pericardium. About 15% of extralobar sequestra are localized in the abdominal cavity, sometimes connecting to the esophagus or stomach. Microscopically: among the pockets of normally formed alveoli there are small but dilated bronchi containing cartilage; in some cases, the dilation of the bronchi is more pronounced, and the alveoli are underdeveloped. Bronchioles and alveolar ducts are irregular in shape. The bronchi are not connected to the tracheobronchial tree. Lymphatic vessels are dilated, which resembles congenital lymphangiectasias. Arterial vessels have a normal structure, but thin-walled vessels can also be found. Due to the lack of normal drainage of the bronchi, secretions stagnate in them, which contributes to infection, cyst formation and fibrosis. Extralobar sequestration can be combined with cystic adenomatous lung disease, types II and III. In 65% of cases, defects of other organs are observed, the most common of which are diaphragmatic hernia, pulmonary hypoplasia, congenital heart disease and pectus excavatum. TTP defect - up to the 6th week of embryonic development.

At intralobar sequestration the abnormal area is usually located in the posterointernal parts of the lower lobe of the left lung among normal lung tissue and is not delimited from the surrounding parenchyma. Rarely combined with other PRs. It is extremely rarely diagnosed in newborns. Occurs with equal frequency in boys and girls. Macroscopically: the abnormal area appears as an atelectatic segment or as polycystic tissue, the cysts are filled with a yellowish-whitish clear fluid or jelly-like masses. Microscopically: the cysts are lined with columnar or cubic epithelium, the lung tissue is underdeveloped. In older children and adults, chronic inflammation with bronchiectasis, fibrosis, and cysts is observed in this area, on the basis of which many authors believe that in older age this is usually an acquired process and rarely congenital.

Infantile (congenital) lobar emphysema (congenital large supertransparent lobe) characterized by stretching of a segment or lobe of the lung due to internal or external obstruction of the bronchi. Boys get sick more often. Clinically diagnosed in newborns with SDD and infants, extremely rarely in older children (acquired emphysema must be excluded), and can cause death. The upper lobes are predominantly affected, rarely - two lobes. The causes of the defect are: stenosis, atresia, abnormal discharge of the bronchi, defects in the development of bronchial cartilage, mucous folds, mucus plugs and aspirated meconium in the bronchial lumen, obstruction of the bronchi by aberrant vessels or bronchogenic cysts, etc. These changes contribute to overstretching of the lung area distal to the site of obstruction due to the fact that when exhaling, less air is removed than enters (valve mechanism). Macroscopically: the affected lobe is enlarged; with sharp swelling, it prolapses through the anterior mediastinum towards the healthy lung, compressing neighboring areas. Microscopically: uniformly overstretched acini with alveolar sacs and alveoli measuring 3-10 times larger than normal are visible, focal ruptures in the alveolar septa are noted. In some cases, this type of emphysema is caused by an increase in the number of alveoli (3-5 times more than normal) in the affected lobe (polyalveolar lobe), while the size of the alveoli does not change. Infantile lobar emphysema is often combined with other defects, especially of the heart. Acquired infantile emphysema is observed in premature infants who were on mechanical ventilation.

Congenital cystic adenomatous lung defect (cystic adenomatous pulmonary dysplasia, cystic adenomatous pulmonary hamartoma)- quite common (accounts for 25% of all congenital lung diseases) hamartomatous lung defect, characterized by the presence of adenomatous proliferating cysts, reminiscent of bronchioles in structure. Cysts are usually connected to the tracheobronchial tree, the blood supply and venous outflow are carried out by normal pulmonary vessels, except in cases of combination with extralobar sequestration. The defect was first described by Ch"in and Tang in 1949. Frequency is 1 case per 25,000-35,000 births. In most cases, it is diagnosed in the first 6 months of life, in 70% - from birth or in the 1st month of life, occasionally later Almost 90% of all observations described in the literature were clinically manifested in children under 2 years of age. In 80% of cases, SDR is clinically observed in varying degrees of severity; in older children, persistent or recurrent pneumonia is present. Currently, the defect is often diagnosed antenatally. mainly in fetuses of 22.6 ± 3 weeks of pregnancy, however, observations in 5-8-week fetuses are described. With antenatal diagnosis, this defect must be differentiated from diaphragmatic hernia, bronchogenic cysts, pulmonary sequestration and congenital lobar emphysema.

The etiology and pathogenesis of this defect are unknown. It is assumed that disruption of normal lung maturation may be due to bronchial atresia or abnormal bronchial division. This leads to dysplasia of the lung tissue distal to the affected segment. The formation of dysplastic lung tissue in the fetus can cause lung hypoplasia or even aplasia. Unlike a normally developing lung, with cystic adenomatous dysplasia there is an increase in cell proliferation and a decrease in the process of apoptosis. In the affected tissue, both in the fetus and in newborns, the expression of some growth factors is increased, in particular platelet-derived growth factor (TFR-BB), glial neurotropic factor (GNTF -GDNF), which are known to be some of the factors that stimulate lung growth and development, and the expression of GDNF in the affected tissue correlates with the degree of proliferation. There is also disintegration in the embryonic period between paracrine factors.

Depending on the clinical manifestations, prognosis and morphology, five types of defect are distinguished.

  • Type 0 - acinar dysplasia - a defect incompatible with life. Combined with heart defects and dermal dysplasia. Macroscopically: the lungs are small, dense, and when cut, the cysts resemble slightly dilated small bronchi. Microscopically: among the abundant mesenchyme there are small (0.5 cm in diameter) bronchiole-like structures lined with high columnar epithelium with mucus-producing goblet cells (mucosal differentiation is unique for this type of defect); the fibromuscular wall contains cartilage and glands.
  • Type I - cystic dysplasia - the most common type (50-75%). It is diagnosed in the 1st week or month of life, but can occur in older children and even adults. Macroscopically: one or many multilocular large cysts (diameter 3-10 cm), filled with air and fluid, surrounded by smaller cysts and compressed normal lung parenchyma. Microscopically: larger cysts are lined with ciliated, pseudomulti-row cylindrical, and smaller cysts are lined with cuboidal or columnar epithelium. In 1/3 of cases, there are mucus-producing cells in the epithelial lining of large cysts or in bronchiolo-alveolar-like structures near the largest cysts. Sometimes, within the cysts and in the adjacent bronchiole-like structures, papillary proliferation of the epithelium is observed, which resembles bronchogenic carcinoma. The wall of cysts consists of elastic, smooth muscle and collagen tissues; in 5-10% of cases cartilage is detected. It is usually treated surgically with a favorable prognosis.
  • Type II - intermediate - the second most common type (about 20-25%). It is observed only in the 1st year of life, has a worse prognosis and is more often combined with other congenital malformations of the heart, central nervous system, urinary, musculoskeletal systems, diaphragmatic hernia, some of them are incompatible with life (for example, arenia, sirenomelia). This type of defect is observed with extralobar sequestration. Macroscopically: the affected part or the entire lung on the section has a spongy appearance and consists of small cysts closely adjacent to each other with a diameter of 0.5 to 2 cm, connecting to the bronchi and filled with air if the child was breathing. The inner surface of the cysts is smooth, shiny or rough. They are evenly distributed among the lung tissue, merging with it. Microscopically: cysts resemble dilated terminal bronchioles, lined with respiratory cubic or columnar epithelium; the wall contains fibrous, elastic and smooth muscle fibers. Mucinous cells and cartilage are absent, but in 5-10% of cases there may be foci of striated muscles (rhabdomyomatous subvariant).
  • Type III - solid - occurs infrequently (5%) and almost only in boys. Pregnancy is complicated by polyhydramnios due to compression of the esophagus by enlarged lobes or the lung. With prolonged compression of the inferior vena cava, hydrops fetalis occurs. In the mother's blood in the 2nd trimester of pregnancy, an increase in the amount of α-feto-protein is observed. Macroscopically: large, dense, tumor-like masses occupy the entire lobe or the entire lung, the mediastinum is always displaced and the affected lung is often hypoplastic (cystic pulmonary hypoplasia). The section reveals small cavities resembling cysts, rarely more than 0.2 cm in diameter (except for scattered, larger bronchiole-like structures). The pulmonary parenchyma outside the cysts is underdeveloped. Microscopically: the affected tissue resembles an immature lung devoid of bronchi. Irregular stellate bronchiole-like structures are lined with cuboidal epithelium and surrounded by alveolar ducts and alveoli, also lined with cuboidal epithelium. Mucous cells and cartilage are absent. The cysts observed in the types described above are absent. The prognosis depends on the extent of the process and the amount of preserved lung tissue, the degree of mediastinal displacement and the presence of congenital malformation. Mortality is high.
  • Type IV - peripheral cystic, distal acinar - occurs in 2-10% of cases. Boys and girls are affected equally often. It is observed in newborns and small children of the first 4 years of life. Macroscopically: large, multilocular, thin-walled, air-containing cysts are localized at the periphery of the lung and can compress other organs of the chest, occasionally complicating pneumothorax. Microscopically, the cysts are lined with flattened alveolar epithelium (type I alveolocytes). The wall consists of dense mesenchymal tissue with clearly visible arteries and arterioles. Mucous cells, cartilage and muscles are absent. The prognosis for surgical treatment is favorable.

Congenital pulmonary lymphangiectasias (lymphangiomatous cysts) are primary and secondary. Secondary ones are caused by obstruction of lymphatic or venous drainage of the lungs, primary ones are an extremely rare defect. Boys are affected 2 times more often. The reasons are heterogeneous. They can be inherited autosomal recessively, but in most cases the defect is sporadic. Often combined with other congenital defects, especially asplenia and heart defects, they are described in Noonan, Turner and Down syndromes. Primary pulmonary lymphangiectasias can be isolated (only the lung is affected) or a manifestation of generalized lymphangiectasias. In newborns, pronounced SDR is clinically observed. In most cases, death occurs within the first hours or days of life, but occasionally they may be first clinically diagnosed only in adults. Macroscopically: the lungs are enlarged, dense, tuberous. In the wide interlobar septa and under the pleura, multiple cysts with a diameter of up to 5 mm are visible, emphasizing the lobar structure of the lungs. Near the hilum of the lungs there are oblong cysts. The contents of the cysts are lymph, or when connected to the bronchi - air and lymph. Microscopically: cysts are localized in the connective tissue under the pleura, in the interlobar septa, near the bronchioles and arteries. Serial sections show that they are part of a complex network of interconnecting lymphatic channels that vary widely in size and lack valves. The cysts are lined with flattened endothelium (markers of the endothelium of lymphatic vessels are CD 31 and factor 8 antigens). In the thin wall, elastic, collagen fibers and rarely smooth muscle cells are detected. The absence of foreign body giant cells in the cyst wall distinguishes this pathology from persistent interstitial emphysema, which is usually a complication of mechanical ventilation in premature infants.

Enterogenous cysts is a form of single-chamber duplication cysts of the gastrointestinal tract. In the chest cavity they are localized in the posterior mediastinum on the right, attached to the esophagus, and rarely connected to the bronchus. Microscopically: the wall of the cyst is lined with multilayered squamous, occasionally gastric or small intestinal epithelium. The gastric epithelium may ulcerate, leading to perforation of the cyst. Enterogenous cysts can be combined with anomalies of the lower cervical and upper thoracic vertebrae.

Capillary alveolar dysplasia- disruption of the structure of the pulmonary vessels. A rare lethal pathology that causes congenital pulmonary hypertension, persistence of fetal circulation and SDR in newborns. Microscopically: the proliferation of connective tissue in the interlobar and interalveolar septa, in which the number of capillaries is reduced, there is no contact between the alveolar epithelium and the capillary. The pulmonary lobules are small, the radial count is reduced. The walls of small arteries are thickened due to hypertrophy of smooth muscle tissue. In addition, there is an abnormal arrangement of the pulmonary veins, which accompany the pulmonary arteries in the center of the acinus, and not in the interlobar septa, as is observed in normal lung tissue. The walls of abnormally located veins are thickened. The causes of the defect are not known. Siblings are rarely affected. May be combined with gastrointestinal and urinary tract defects.

Pulmonary arteriovenous fistulas- abnormal communications between arteries and veins. The process is most often localized in the lower lobe. It is observed in 25% of patients with Randu-Weber-Osler disease (familial hemorrhagic telangiectasia) - an autosomal dominant hereditary disease with high penetrance. Homozygous forms are in some cases lethal in early childhood.

Congenital surfactant deficiency (congenital alveolar proteinosis)

This is an autosomal recessive hereditary deficiency of one of the surfactant proteins - surfactant protein B (SP-B), caused by a mutation in codon 121 of the SP-B gene and its RNA - SP-B mRNA. Clinically characterized by rapidly progressing respiratory failure immediately after birth. Macroscopically: the lungs are dense, more than 2 times enlarged, airless. Microscopically: the alveoli are dilated, lined with cuboidal epithelium and filled with eosinophilic, granular, PAS positive masses with desquamated alveolocytes and an abundance of macrophages. In the final stage, thickening of the alveolar septa is observed due to the proliferation of fibroblasts. Immunohistochemically, the absence or reduction of surfactant protein is determined with normal amounts of proteins A and C. The prognosis is unfavorable. In all cases described in the literature, death occurred within the 1st year of life.

Primary pulmonary hypertension

Hypertension of the pulmonary circulation in newborns can be associated with the persistence of the fetal arteries of the lungs, hypertrophy of their muscular layer, proliferation and fibrosis of the intima, sometimes fibrinoid necrosis and arteritis, which leads to precapillary obstruction of the branches of the pulmonary artery and the formation of secondary glomus anastomoses. With this variant, the disease occurs in a fulminant manner, and children die in the first months of life. Sudden death is often observed. Hypertrophy of the muscular lining of the pulmonary vessels (mainly small intraacinar arteries) is also observed with intrauterine asphyxia, pulmonary hypoplasia, premature closure of the ductus arteriosus, and diaphragmatic hernia.

Benign familial pneumothorax

It is extremely rare in newborns and is mainly observed in adolescent males. Families with both autosomal dominant and autosomal recessive types of inheritance have been described.

The embryonic period of fetal development, unfortunately, does not always pass without problems. All kinds of intrauterine developmental defects sometimes occur for no apparent reason. And one of these fetal developmental defects is pulmonary aplasia, characterized by unformed lungs and the presence of a rudimentary bronchus. This defect can affect either one lung or both at once. In the case where one lung is missing, the newborn has every chance of a normal life. The absence of both lungs is a developmental defect incompatible with life. As a rule, a child born without lungs dies before birth, but in some cases he can live for some time after birth (maximum several hours). Pulmonary aplasia refers not only to the complete absence of a lung or lungs: aplasia is also commonly called a pathology such as the absence of a part of the lung, that is, its certain lobes.

As a rule, pulmonary aplasia is a disease that is accompanied by other abnormalities in the development of the body. Most often, together with pulmonary aplasia, the patient may experience heart disease, chest degeneration, anencephaly, diaphragmatic hernia, abnormalities of the kidneys and urinary tract, and more. Of course, the more concomitant diseases and malformations of pulmonary aplasia, the less chance the patient has to survive. And the point is not even that these diseases are difficult to cure, but that newborns with a large number of defects are born very weak and their body cannot help the medical influence exerted on it.

Pulmonary aplasia is a dangerous disease also because the affected organs are very susceptible to infections that affect the respiratory system. That is, the same influenza virus or a common ARVI, relatively calmly tolerated by a healthy person, can become deadly for a person suffering from pulmonary aplasia.

Clinical picture of the disease

In patients who have underdeveloped or absent lungs, clinical manifestations can be very diverse. In addition, the disease can often be asymptomatic. There are cases when pulmonary aplasia is detected completely by accident, for example, during a preventive x-ray examination. But such cases are rather rare than regular. Most often, the clinical symptoms of pulmonary aplasia are detected in the first years of the patient’s life. The main symptom of aplasia is the tendency of the respiratory organs to become infected, in which inflammatory processes form not only in the organ affected by aplasia, but also in a healthy, normally developed organ. Frequent pulmonary diseases and layers of infections often cause the formation of secondary chronic pneumonia. It is not uncommon for patients with aplasia to have a cough, accompanied by the discharge of sputum mixed with pus, as well as shortness of breath. Moreover, shortness of breath can appear not only as a result of physical activity, but also for no reason. Very often, patients with pulmonary aplasia complain of periodically recurring chest pain.

Underdevelopment of the lung usually affects the physical development of the patient. The presence of aplasia can be visually assumed by the patient’s deformed chest, which is narrowed and flatter on the side where the respiratory organ is absent. The depression of the chest is especially noticeable in patients with agenesis, a disease very similar in its morphological structure to aplasia. Sometimes patients with aplasia exhibit thickening of the nail phalanges of the fingers - an anomaly known under the medical term “clubs”.

Diagnosis of aplasia

When examining a patient with aplasia using X-ray equipment, the doctor may note a sharp shift towards the mediastinal anomaly, in which only the lower part of the hemithorax remains obscured. While in the upper part, transparent lung tissue is visible, due to the prolapse of the existing lung through the lower part of the mediastinum. Sometimes such a picture can give rise to the false impression that both lungs are present, one of which is supposedly simply reduced in size. A more accurate diagnosis can be obtained by undergoing a tomographic examination, which gives a more complete picture. The most reliable information can be obtained from bronchography.

Treatment of pulmonary aplasia

This anomaly of intrauterine development of the fetus is not subject to surgical treatment. However, there is no other specific treatment for this disease.
Treatment of patients consists of implementing supportive measures, consisting of artificial ventilation and additional oxygen supply to the patient. This supportive treatment is aimed at creating sufficient conditions for the lung to grow and ensure the patient's survival. A mandatory condition for the life of a patient with aplasia is annual vaccination against the influenza virus and taking antibiotics to combat infections that affect the main human respiratory organ.

In general, in the absence of a large number of additional defects, people with aplasia can live quite a long time. However, it is quite difficult to call their life full, since they need to pay special attention not only to their health, but also to employment and lifestyle. There are cases where patients with aplasia lived to be 60 years or more.

Focal formations in the lungs are tissue compactions, which can be caused by various ailments. Moreover, to establish an accurate diagnosis, a doctor’s examination and radiography are not enough. The final conclusion can be made only on the basis of specific examination methods, including blood tests, sputum tests, and tissue puncture.

Important: the opinion that only tuberculosis can be the cause of multiple focal lung lesions is erroneous.

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Therefore, the diagnosis must be preceded by a thorough examination of the patient. Even if the doctor is sure that a person has focal pneumonia, it is necessary to perform a sputum analysis. This will identify the pathogen that caused the development of the disease.

Now some patients refuse to undergo certain specific tests. The reason for this may be reluctance or inability to visit the clinic due to its distance from the place of residence, or lack of funds. If this is not done, then there is a high probability that focal pneumonia will become chronic.

What are foci and how to identify them?

Now focal formations in the lungs are divided into several categories based on their number:

  1. Singles.
  2. Single – up to 6 pieces.
  3. Multiple – dissemination syndrome.

There is a difference between the internationally accepted definition of what lung lesions are and what is accepted in our country. Abroad, this term refers to the presence of areas of compaction in the lungs of a round shape and a diameter of no more than 3 cm. Domestic practice limits the size to 1 cm, and the remaining formations are classified as infiltrates, tuberculomas.

Important: a computer examination, in particular tomography, will allow you to accurately determine the size and shape of the lesion in the lung tissue. However, it is necessary to understand that this examination method also has its own error threshold.

In fact, a focal formation in the lung is a degenerative change in the lung tissue or the accumulation of fluid (sputum, blood) in it. Correct characterization of single pulmonary lesions (SLP) is one of the most important problems of modern medicine.

The importance of the task lies in the fact that 60-70% of such formations that were cured, but then reappeared, are malignant tumors. Among the total number of AOLs identified during MRI, CT or radiography, their portion is less than 50%.

An important role here is played by how lesions in the lungs are characterized on CT. Using this type of examination, based on characteristic symptoms, the doctor can make assumptions about the presence of serious diseases such as tuberculosis or malignant neoplasms.

However, to clarify the diagnosis, additional tests are necessary. A hardware examination is not enough to issue a medical report. Until now, everyday clinical practice does not have a unified algorithm for differential diagnosis for all possible situations. Therefore, the doctor considers each case separately.

Tuberculosis or pneumonia? What can prevent, with the modern level of medicine, from making an accurate diagnosis using the hardware method? The answer is simple - imperfect equipment.

In fact, when undergoing fluorography or radiography, it is difficult to identify OOL, the size of which is less than 1 cm. Interposition of anatomical structures can make larger lesions practically invisible.

Therefore, most doctors advise patients to give preference to computed tomography, which makes it possible to view tissue in section and from any angle. This completely eliminates the possibility that the lesion will be obscured by the cardiac shadow, ribs, or roots of the lungs. That is, radiography and fluorography simply cannot consider the whole picture as a whole and without the possibility of a fatal error.

It should be taken into account that computed tomography can detect not only AOL, but also other types of pathologies, such as emphysema and pneumonia. However, this examination method also has its weaknesses. Even with a CT scan, focal formations may be missed.

This has the following explanations for the low sensitivity of the device:

  1. The pathology is in the central zone – 61%.
  2. Size up to 0.5 cm – 72%.
  3. Low fabric density – 65%.

It has been established that with a primary screening CT scan, the probability of missing a pathological change in tissue, the size of which does not exceed 5 mm, is about 50%.

If the diameter of the lesion is more than 1 cm, then the sensitivity of the device is more than 95%. To increase the accuracy of the obtained data, additional software is used to obtain 3D images, volumetric rendering and maximum intensity projections.

Anatomical features

In modern domestic medicine, there is a gradation of lesions based on their shape, size, density, structure and condition of the surrounding tissues.

An accurate diagnosis based on CT, MRI, fluorography or radiography is possible only in exceptional cases.

Usually in the conclusion only the probability of the presence of a particular disease is given. In this case, the location of the pathology itself is not given decisive importance.

A striking example is the presence of a lesion in the upper lobes of the lung. It has been established that this localization is characteristic of 70% of cases of detection of a primary malignant tumor of this organ. However, this is also typical for tuberculous infiltrates. With the lower lobe of the lung there is approximately the same picture. Here, cancer that has developed against the background of idiopathic fibrosis and pathological changes caused by tuberculosis are detected.

Great importance is given to the contours of the lesions. In particular, a fuzzy and uneven outline, with a lesion diameter of more than 1 cm, signals a high probability of a malignant process. However, if clear margins are present, this is not sufficient reason to stop diagnosing the patient. This picture is often present in benign neoplasms.

Particular attention is paid to tissue density: based on this parameter, the doctor is able to distinguish pneumonia from scarring of lung tissue, for example, caused by post-tuberculosis changes.

The next nuance is that CT allows you to determine the types of inclusions, that is, determine the structure of the OOL. In fact, after an examination, a specialist can say with high accuracy what kind of substance accumulates in the lungs. However, only fatty inclusions make it possible to determine the ongoing pathological process, since all the others do not belong to the category of specific symptoms.

Focal changes in the lung tissue can be provoked by both a fairly easily treatable disease - pneumonia, and more serious ailments - malignant and benign neoplasms, tuberculosis. Therefore, it is important to identify them in a timely manner, in which a hardware examination method - computed tomography - will help.

Lung diseases develop against the background of the penetration of pathogenic microbes into the body, often caused by smoking and alcoholism, poor ecology, and harmful production conditions. Most diseases have a pronounced clinical picture and require immediate treatment, otherwise irreversible processes begin to occur in the tissues, which can lead to severe complications and death.

Lung diseases require immediate treatment

Classification and list of lung diseases

Lung diseases are classified depending on the localization of the inflammatory, destructive process - pathologists can affect blood vessels, tissues, and spread to all respiratory organs. Diseases in which it is difficult for a person to take a full breath are called restrictive, while diseases in which it is difficult for a person to take a full breath are called obstructive.

According to the degree of damage, pulmonary diseases are local and diffuse, all respiratory diseases have an acute and chronic form, pulmonary pathologies are divided into congenital and acquired.

General signs of bronchopulmonary diseases:

  1. Shortness of breath occurs not only during physical activity, but also at rest, against the background of stress; a similar symptom occurs with heart disease.
  2. Cough is the main symptom of respiratory tract pathologies; it can be dry or wet, barking, paroxysmal, the sputum often contains a lot of mucus, inclusions of pus or blood.
  3. A feeling of heaviness in the chest, pain when inhaling or exhaling.
  4. Whistling, wheezing when breathing.
  5. Fever, weakness, general malaise, loss of appetite.

Most of the problems associated with the respiratory system are combined diseases; several parts of the respiratory system are affected at once, which greatly complicates diagnosis and treatment.

A feeling of heaviness in the chest indicates lung disease

Pathologies that affect the respiratory tract

These diseases have a pronounced clinical picture and are difficult to treat.

COPD

Chronic obstructive pulmonary disease is a progressive disease in which structural changes occur in the vessels and tissues of the organ. Most often diagnosed in men over 40 years of age, heavy smokers, the pathology can cause disability or death. The ICD-10 code is J44.

Healthy lungs and lungs with COPD

Symptoms:

  • chronic wet cough with a lot of sputum;
  • severe shortness of breath;
  • when exhaling, the volume of air decreases;
  • in the later stages, cor pulmonale and acute respiratory failure develop.
The reasons for the development of COPD are smoking, ARVI, bronchial pathologies, harmful production conditions, polluted air, genetic factor.

It is a type of COPD and often develops in women due to hormonal imbalance. ICD-10 code – J43.9.

Emphysema most often develops in women

Symptoms:

  • cyanosis - the nail plates, the tip of the nose and earlobes acquire a blue tint;
  • shortness of breath with difficulty exhaling;
  • noticeable tension in the diaphragm muscles when inhaling;
  • swelling of the veins in the neck;
  • weight loss;
  • pain in the right hypochondrium, which occurs when the liver is enlarged.

Feature – when coughing, a person’s face turns pink, and during an attack a small amount of mucus is released. As the disease progresses, the patient's appearance changes - the neck becomes shorter, the supraclavicular fossa protrudes strongly, the chest becomes rounded, and the abdomen sags.

Asphyxia

The pathology occurs against the background of damage to the respiratory organs, chest injuries, and is accompanied by increasing suffocation. The ICD-10 code is T71.

Symptoms:

  • at the initial stage - rapid shallow breathing, increased blood pressure, palpitations, panic, dizziness;
  • then the breathing rate decreases, exhalation becomes deep, pressure decreases;
  • Gradually, arterial indicators decrease to critical levels, breathing is weak, often disappears, the person loses consciousness, may fall into a coma, and pulmonary and cerebral edema develops.

An attack of suffocation can be triggered by the accumulation of blood, sputum, vomit in the respiratory tract, suffocation, an attack of allergies or asthma, or a burn of the larynx.

The average duration of an attack of asphyxia is 3–7 minutes, after which death occurs.

A viral, fungal, bacterial disease that often becomes chronic, especially in children, pregnant women, and the elderly. The ICD-10 code is J20.

Symptoms:

  • nonproductive cough – appears at the initial stage of disease development;
  • wet cough is a sign of the second stage of the disease, the mucus is transparent or yellow-green in color;
  • temperature rise to 38 degrees or more;
  • increased sweating, weakness;
  • shortness of breath, wheezing.

Bronchitis often becomes chronic

The development of the disease can be provoked by:

  • inhalation of dirty, cold, damp air;
  • flu;
  • cocci;
  • smoking;
  • avitaminosis;
  • hypothermia.

A rare systemic disease that affects various organs, often affecting the lungs and bronchi, and is diagnosed in people under 40 years of age, more often in women. It is characterized by accumulations of inflammatory cells called granulomas. The ICD-10 code is D86.

In sarcoidosis, there is an accumulation of inflammatory cells

Symptoms:

  • severe fatigue immediately after waking up, lethargy;
  • loss of appetite, sudden weight loss;
  • temperature rise to subfebrile levels;
  • nonproductive cough;
  • muscle and joint pain;
  • dyspnea.

The exact causes of the development of the disease have not yet been identified; many doctors believe that granulomas are formed under the influence of helminths, bacteria, pollen, and fungi.

Diseases in which the alveoli are damaged

Alveoli are small bubbles in the lungs that are responsible for gas exchange in the body.

Pneumonia is one of the most common pathologies of the respiratory system, often developing as a complication of influenza and bronchitis. The ICD-10 code is J12–J18.

Pneumonia is the most common lung disease

Symptoms of pathology depend on its type, but there are general signs that appear at the initial stage of development of the disease:

  • fever, chills, fever, runny nose;
  • severe cough - at the initial stage it is dry and persistent, then it becomes wet, green-yellow sputum with impurities of pus is released;
  • dyspnea;
  • weakness;
  • chest pain when taking a deep breath;
  • cephalgia.

There are many reasons for the development of infectious pneumonia - the disease can be provoked by gram-positive and gram-negative bacteria, mycoplasma, viruses, and Candida fungi. The non-infectious form of the disease develops due to inhalation of toxic substances, burns of the respiratory tract, blows and bruises of the chest, against the background of radiation therapy and allergies.

Tuberculosis

A fatal disease in which lung tissue is completely destroyed, the open form is transmitted by airborne droplets, you can also become infected by consuming raw milk, the causative agent of the disease is the tuberculosis bacillus. The ICD-10 code is A15–A19.

Tuberculosis is a very dangerous disease

Signs:

  • cough with phlegm that lasts more than three weeks;
  • presence of blood in mucus;
  • prolonged increase in temperature to subfebrile levels;
  • chest pain;
  • night sweats;
  • weakness, weight loss.

Tuberculosis is often diagnosed in people with weakened immune systems; the development of the disease can be triggered by a deficiency of protein foods, diabetes mellitus, pregnancy, and alcohol abuse.

The disease develops when interstitial fluid from blood vessels penetrates into the lungs and is accompanied by inflammation and swelling of the larynx. The ICD-10 code is J81.

When swelling occurs, fluid accumulates in the lungs

Causes of fluid accumulation in the lungs:

  • acute heart failure;
  • pregnancy;
  • cirrhosis;
  • starvation;
  • infectious diseases;
  • intense physical activity, climbing to great heights;
  • allergy;
  • sternum injuries, presence of a foreign body in the lungs;
  • Edema can be provoked by the rapid administration of a large amount of saline solution or blood substitutes.

At the initial stage, shortness of breath, dry cough, increased sweating, and increased heart rate appear. As the disease progresses, foamy pink sputum begins to be released when coughing, breathing becomes wheezing, the veins in the neck swell, the limbs become cold, the person suffers from suffocation, and loses consciousness.

Acute respiratory syndrome is a rare but very dangerous disease that is practically untreatable; a person is connected to a ventilator.

Carcinoma is a complex disease, in the final stages of development it is considered incurable. The main danger of the disease is that in the early stages of development it is asymptomatic, so people go to the doctor with advanced forms of cancer, when there is complete or partial drying out of the lung and tissue decomposition. The ICD-10 code is C33–C34.

Lung cancer often has no symptoms

Symptoms:

  • cough – sputum contains blood clots, pus, mucus;
  • dyspnea;
  • chest pain;
  • dilatation of veins in the upper chest, jugular vein;
  • swelling of the face, neck, legs;
  • cyanosis;
  • frequent attacks of arrhythmia;
  • sudden weight loss;
  • fatigue;
  • unexplained fever.
The main cause of cancer development is active and passive smoking, work in hazardous industries.

Diseases that affect the pleura and chest

The pleura is the outer lining of the lungs, similar to a small sac; some serious diseases develop when it is damaged; often the organ simply collapses and the person cannot breathe.

The inflammatory process occurs against the background of injury or penetration of pathogenic microorganisms into the respiratory system. The disease is accompanied by shortness of breath, pain in the chest area, and a dry cough of moderate intensity. ICD-10 code – R09.1, J90.

With pleurisy, the lungs are affected by harmful microorganisms

Risk factors for the development of pleurisy are diabetes, alcoholism, rheumatoid arthritis, chronic diseases of the digestive system, in particular, bending of the colon.

People who work at chemical plants for a long time often develop an occupational lung disease in mines - silicosis. The disease progresses slowly, in the final stages there is a strong increase in temperature, incessant cough, and breathing problems.

Air enters the pleural area, which can cause collapse; immediate medical attention is required. The ICD-10 code is J93.

Pneumothorax requires prompt intervention

Symptoms:

  • frequent shallow breathing;
  • cold clammy sweat;
  • bouts of unproductive cough;
  • the skin takes on a blue tint;
  • the heart rate increases, blood pressure decreases;
  • fear of death.

Spontaneous pneumothorax is diagnosed in tall men, smokers, and with a sharp drop in pressure. The secondary form of the disease develops with long-term diseases of the respiratory system, cancer, against the background of injuries to the connective tissue of the lungs, rheumatoid arthritis, and scleroderma.

Pulmonary hypertension is a specific syndrome of obstructive bronchitis, fibrosis, develops more often in older people, and is characterized by increased pressure in the vessels that supply the respiratory organs.

Purulent diseases

Infections affect a significant part of the lungs, which causes the development of severe complications.

An inflammatory process in which a cavity with purulent contents forms in the lungs; the disease is difficult to diagnose. The ICD-10 code is J85.

Abscess - purulent formation in the lungs

Reasons:

  • insufficient oral hygiene;
  • alcohol, drug addiction;
  • epilepsy;
  • pneumonia, chronic bronchitis, sinusitis, tonsillitis, carcinoma;
  • reflux disease;
  • long-term use of hormonal and antitumor drugs;
  • diabetes, cardiovascular pathologies;
  • chest injuries.

In the acute form of an abscess, the clinical picture is clearly intense pain in the chest, most often on one side, prolonged bouts of wet cough, blood and mucus are present in the sputum. As the disease progresses to the chronic stage, exhaustion, weakness, and chronic fatigue occur.

A fatal disease - against the background of a putrefactive process, the lung tissue disintegrates, the process quickly spreads throughout the body, the pathology is more often diagnosed in men. The ICD-10 code is J85.

Lung gangrene - decomposition of lung tissue

Symptoms:

  • the disease develops quickly, there is a rapid deterioration in health;
  • pain in the sternum when taking a deep breath;
  • a sharp increase in temperature to critical levels;
  • severe cough with a lot of foamy sputum - the discharge has a foul odor and contains brown streaks of blood and pus;
  • suffocation;
  • increased sweating;
  • increased heart rate;
  • the skin becomes pale.
The only reason for the development of gangrene is damage to the lung tissue by various pathogenic microorganisms.

Hereditary diseases

Diseases of the respiratory system are often inherited; they are diagnosed in children immediately after birth, or during the first three years of life.

List of hereditary diseases:

  1. Bronchial asthma – develops against the background of neurological pathologies and allergies. Accompanied by frequent severe attacks during which it is impossible to fully inhale and shortness of breath.
  2. Cystic fibrosis - a disease accompanied by excessive accumulation of mucus in the lungs, affects the glands of the endocrine system, and negatively affects the functioning of many internal organs. Against this background, bronchiectasis develops, which is characterized by a constant cough with the release of thick purulent sputum, shortness of breath and wheezing.
  3. Primary dyskinesia is congenital purulent bronchitis.

Many lung malformations can be seen during ultrasound during pregnancy and intrauterine treatment can be performed.

Bronchial asthma is inherited

Which doctor should I contact?

If symptoms of a pulmonary disease appear, you should visit a physician or pediatrician. After listening and preliminary diagnosis, the doctor will give a referral to a pulmonologist. In some cases, consultation with an oncologist or surgeon may be required.

The doctor can make a primary diagnosis after an external examination, during which they perform palpation, percussion, and listen to the sounds of the respiratory organs using a stethoscope. To recognize the true cause of the development of the disease, it is necessary to conduct laboratory and instrumental studies.

Basic diagnostic methods:

  • general blood and urine analysis;
  • examination of sputum to identify hidden impurities and pathogenic microorganisms;
  • immunological research;
  • ECG - allows you to determine how a pulmonary disease affects the functioning of the heart;
  • bronchoscopy;
  • chest x-ray;
  • fluorography;
  • CT, MRI – allows you to see changes in the structure of tissues;
  • spirometry – using a special device, the volume of inhaled and exhaled air and the inhalation rate are measured;
  • sounding - a method necessary for studying respiratory mechanics;
  • surgical methods - thoracotomy, thoracoscopy.

Chest X-ray helps to see the condition of the lungs

All pulmonary diseases require serious drug therapy, often treated in a hospital setting. You should immediately consult a doctor if there are specks or blood clots in the sputum.

Treatment of lung diseases

Based on the diagnostic results obtained, the specialist draws up a treatment regimen, but in any case, therapy uses an integrated approach that is aimed at eliminating the causes and symptoms of the disease. Most often, doctors prescribe medications in the form of tablets, suspensions and syrups; in severe patients, drugs are administered by injection.

Groups of drugs:

  • antibiotics of the penicillin, macrolide, cephalosporin group - Cefotaxime, Azithromycin, Ampicillin;
  • antiviral drugs – Remantadine, Isoprinosine;
  • antifungal agents – Nizoral, Amphoglucamine;
  • anti-inflammatory drugs - Indomethacin, Ketorolac;
  • medicines to eliminate dry cough - Glauvent;
  • mucolytics - Glyciram, Broncholitin; Carbocisteine ​​is considered the most effective for the treatment of childhood diseases;
  • bronchodilators to eliminate bronchospasm - Eufillin, Salbutamol;
  • anti-asthma drugs – Atma, Solutan;
  • – Ibuprofen, Paracetamol.

Atma - a remedy for asthma

Additionally, vitamin complexes, immunostimulants, physiotherapy, and traditional medicine are prescribed. In complex and advanced forms of the disease, surgical intervention is required.

To speed up the healing process, it is necessary to include in the diet foods high in ascorbic acid, vitamin E, B1, B2.

Possible complications

Without proper treatment, pathologies of the respiratory system become chronic, which is fraught with constant relapses at the slightest hypothermia.

Why are lung diseases dangerous?

  • asphyxia;
  • against the background of narrowing of the lumen of the respiratory tract, hypoxia develops, all internal organs suffer from a lack of oxygen, which negatively affects their work;
  • an acute asthma attack can be fatal;
  • serious heart disease develops.

An acute asthma attack is deadly

Pneumonia ranks second among diseases that end in death - this is due to the fact that most people ignore the symptoms of the disease. At the initial stage, the disease can be easily cured in 2–3 weeks.

Prevention of pulmonary diseases

To reduce the risk of developing respiratory diseases and their complications, it is necessary to strengthen the immune system, lead a healthy lifestyle, and when the first alarming signs appear, you should consult a specialist.

How to avoid problems with the lungs and bronchi:

  • give up addictions;
  • avoid hypothermia;
  • spend more time outdoors;
  • maintain optimal temperature and humidity in the room, regularly do wet cleaning;
  • play sports, take a contrast shower, get enough sleep, avoid stress;
  • eat healthy and wholesome food, maintain a drinking regime;
  • every year undergo an examination, do a lung x-ray or fluorography.

Walking in the fresh air is good for your health

Breathing sea and pine air has a beneficial effect on the organs, so every year it is necessary to relax in the forest or on the sea coast. During cold epidemics, take antiviral drugs for prevention, avoid crowded places, and limit contact with sick people.

Lung diseases can cause death; timely diagnosis and regular preventive examinations will help to avoid the disease, or begin treatment at the initial stage of development of the pathology.