Diseases of the trachea and bronchi: causes, symptoms, diagnosis, treatment

Depending on their type, diseases of the trachea and bronchi may be the responsibility of a family doctor, general practitioner, pulmonologist, allergist, endoscopist, thoracic surgeon, and even a geneticist. These diseases are not directly related to an otolaryngologist, however, there are cases when patients come to him with complaints that may be caused by damage to both the larynx and trachea. In these cases, an ENT specialist must have basic information about diseases of the trachea and bronchi, be able to differentiate the main nosological forms in relation to diseases of the larynx, trachea and bronchi, provide first aid for these diseases and refer the patient to the appropriate specialist for consultation. Basic information about diseases of the trachea and bronchi includes signs of dysfunction of the main functions of the lower respiratory tract, which include dysfunction of the airway, motor, and secretory functions.

The main functional disorder in various pathological conditions of the trachea and bronchi, causing obstacles to the air flow, is dyspnea. This concept implies modifications of the respiratory function, manifested in changes in the frequency, rhythm and depth of breathing.

Dyspnea occurs when the lower respiratory tract, due to certain pathological conditions, cannot provide full oxygenation of the body and the removal of carbon dioxide from it. The accumulation of carbon dioxide in the blood is controlled by the respiratory and vasomotor centers. An increase in its concentration causes an increase in the frequency and depth of respiratory movements, an increase in the heart rate. These phenomena increase the flow rate of respiratory air passing through the alveolar system and increase the concentration of oxygen in the blood. An important role in the regulation of respiratory function and cardiac activity is also played by vascular interoreceptors, in particular, the carotid glomeruli. All these mechanisms function quite fully when the tracts are free for the air stream, but when they are obstructed, the supply of oxygen to the body and the removal of carbon dioxide from it are insufficient, and then asphyxia occurs due to the hypoxia factor.

In clinical terms, there are different forms (types) of hypoxia: hypoxic hypoxia (lack of oxygen in the inhaled air (for example, when climbing to a high altitude), respiratory hypoxia (in diseases of the lungs and respiratory tract), hemic hypoxia (in diseases of the blood, in particular in anemia, blood loss and some poisonings, for example, in poisoning with carbon monoxide, nitrates), circulatory hypoxia (in circulatory disorders), tissue or cellular hypoxia (in disorders of tissue respiration, for example, in cyanide poisoning, in some metabolic diseases. Most often, hypoxia is of a mixed nature.

Hypoxic hypoxia occurs when the hemoglobin molecule is insufficiently saturated with oxygen, which can be caused by various reasons and most often by pathological conditions of the external respiratory system (paralysis of the respiratory center; myasthenia, blocking the function of the respiratory muscles; obstruction of the respiratory tract by internal and external tumor and edematous-inflammatory processes, injuries, etc.). Hypoxic hypoxia can occur during anesthesia, exudative pleurisy, mediastinal emphysema and pneumothorax, or with a decrease in the respiratory surface of the alveoli (pneumonia, atelectasis, pneumosclerosis, pulmonary emphysema. Hypoxic hypoxia is often combined with other types of hypoxia, which is determined by the corresponding pathological changes in the central nervous system, body tissues, cardiovascular system activity, blood loss, etc.

Disruption of the airway function in the trachea and bronchi can be caused by mechanical, inflammatory, traumatic and neurogenic factors.

Mechanical or obstructive factors may be caused by foreign bodies in the trachea and bronchi, internal volumetric processes (infectious granulomas, tumors), external volumetric processes (tumors, emphysema, mediastinal phlegmon), etc. Complete stenosis of the trachea, main and primary bronchi occurs extremely rarely, but complete stenosis of smaller bronchi often occurs, as a result of which, within a few hours, air from the corresponding lobe of the lung is absorbed and replaced by transudate, after the absorption of which atelectasis of this part of the lung occurs.

Incomplete bronchial stenosis may occur with or without a valve mechanism, and the existing valve "works" in only one direction: it lets air through either only during inhalation or only during exhalation. If the valve prevents air from entering the underlying bronchi (inspiratory valve), then the resorption of air in them leads to atelectasis of the corresponding part of the lung; with an expiratory valve, overflow of the underlying bronchi and lung tissue with air (emphysema) occurs. The valve mechanism may be caused by mobile tumors, their fragments, mobile foreign bodies, etc. With an expiratory valve, due to overflow of the lung tissue with air, it may rupture with the formation of air sacs. With an incomplete valve mechanism, the phenomenon of hypoventilation is observed, which can occur according to the inspiratory or expiratory type and be accompanied, respectively, by collapse of the lung tissue or its emphysema.

Tracheal stenosis is similar to laryngeal stenosis in its clinical manifestations, with the exception that laryngeal stenosis is also accompanied by pronounced aphonia, while tracheal stenosis leaves the voice clear but weakened. Complete acute tracheal stenosis leads to immediate suffocation and death of the patient within 5-7 minutes. Incomplete stenosis causes the development of hypoxic hypoxia, adaptation to which depends on the degree of stenosis and the rate of its development.

Obstructive factors causing hypoxia include edematous and infiltrative processes developing during banal and specific inflammations. This also includes obstructive phenomena caused by bronchospasm in asthmatic conditions, as well as allergic edema of the mucous membrane and submucous layer of the tracheobronchial tree.

Traumatic factors causing dyspnea include mechanical, chemical and thermal agents causing damage to the mucous membrane and submucous layer of the trachea and bronchi of varying severity (both in prevalence and depth). Mechanical factors include foreign bodies in the trachea and bronchi, gunshot wounds, chest contusions and compressions, which cause ruptures and tears of these organs, crushing of lung tissue, damage to the organs of the mediastinum and spine. These factors should also include iatrogenic damage that occurs during tracheo- and bronchoscopy, when removing foreign bodies, etc. The mechanism of chemical and physical damage to the trachea and bronchi is identical to that which occurs when these factors damage the larynx and invariably accompanies it.

Neurological diseases can play an important role in the pathogenesis of dyspnea, in which various lesions of the peripheral nerves innervating the trachea and bronchi, or central structures regulating the muscle tone of these organs occur. These disorders, concerning the motor nerves, cause motor disorders - vegetative nerves - trophic disorders and, above all, secretory function. The latter are reflected in quantitative and qualitative changes in the production of mucous glands of the lower respiratory tract, and the motor function of the ciliated epithelium changes significantly, which disrupts excretion, i.e., the evacuation function.

Hypersecretion is a protective response to any inflammatory process, ensuring the washing out of catabolites, dead leukocytes and microbial bodies, but excessive accumulation of mucus reduces the activity of the ciliated epithelium's sewage function, and the mucus itself in large quantities begins to play the role of a volumetric factor that enhances the phenomenon of hypoxic hypoxia. In addition, the greenhouse effect created in this case promotes the proliferation of microbiota and the strengthening of secondary infection. Thus, hypersecretion leads to the creation of a vicious circle that aggravates the pathological condition of this organ.

Hyposecretion occurs with atrophic processes in the mucous membrane and its elements (ozena, scleroma, silicosis and other professional dystrophies of the respiratory tract). Hyposecretion is the result of hypotrophy of morphological elements not only of the mucous membranes of the respiratory tract, but also of their cartilaginous skeleton and other elements of these organs (smooth muscles, nervous and lymphadenoid apparatus).

The basis of the excretion disorder is the hypofunction of mucociliary clearance, the complete disappearance of which, caused by purulent-inflammatory or neoplastic processes, leads to bronchopulmonary stasis - the main cause of the occurrence of inflammatory processes in the lower respiratory tract.

Tracheobronchial syndromes. Tracheobronchial syndromes are largely determined by the topographic-anatomical relationship with the organs of the neck and mediastinum, which can significantly affect the state of the lumen of the trachea and bronchi when various diseases occur in these organs. The trachea, due to its anatomical position, makes excursions both in the lateral and vertical directions; it transmits the movements of the lungs, aorta, esophagus, and spine. Such an active influence of neighboring organs on the trachea and bronchi often significantly modifies the functions of the latter and complicates differential diagnostics between diseases of the chest organs. Thus, pathological conditions observed in the upper trachea can simulate or be associated with diseases of the larynx, similar diseases of the trachea in the lower sections, especially in the bifurcation area, often take on the aspect of bronchopulmonary diseases, and lesions in the middle sections of the trachea can be taken for diseases of neighboring organs located at this level, especially the esophagus. Similar aspects of the difficulties of differential diagnostics of diseases of the tracheobronchial system fully concern the bronchi. Knowledge of the signs of tracheal and bronchial syndromes provides significant assistance in this problem.

Tracheal syndromes are divided into high, middle and low.

High tracheal syndromes are characterized by a soreness and tickling in the larynx and upper trachea. The patient assumes a forced position with the head tilted forward, which relaxes the trachea and increases its elasticity and compliance. This position should be distinguished from the forced position that occurs with dyspnea of laryngeal origin, in which the patient tilts the head back to facilitate chest breathing. In diseases of the upper trachea, phonation is impaired only when the lower laryngeal (recurrent) nerves are involved in the pathological process.

Average tracheal syndromes are characterized only by signs of tracheal damage. The most typical symptom is cough, which owes its origin to irritation of the sensory nerves of the trachea. It is paroxysmal, sometimes uncontrollable in nature and can be a sign of both acute banal inflammatory diseases and specific and neoplastic processes. In banal processes, at the onset of the disease, a "dry" cough is especially painful, then with the appearance of sputum, the intensity of soreness, pain and tickling decreases. Dyspnea in this syndrome occurs when the pathological process is characterized by a sign of tracheal obstruction and a decrease in its airway function. Shortness of breath and signs of hypoxic hypoxia in these cases at the onset of the disease can manifest themselves only with physical exertion, but after this, these phenomena do not pass for a long time due to a latent oxygen deficiency in the body. As the pathological process increases (edema, infiltration, compression by a growing tumor of the esophagus, mediastinal emphysema, etc.), dyspnea increases and becomes constant even in a state of physical rest.

In anterior tracheal syndromes, dyspnea increases at night and is accompanied by noisy breathing. The patient suddenly wakes up during an attack of suffocation with a frightened expression, the face is cyanotic, breathing and pulse are rapid. These nocturnal excesses often simulate asthma. Tracheal dyspnea is accompanied by snoring, but unlike laryngeal dyspnea, in which snoring occurs only on inhalation, with tracheal dyspnea it occurs on inhalation and exhalation. Involvement of the recurrent nerves in the process can manifest itself as a tonal voice disorder, a characteristic sign of which is an involuntary transition from a normal tone to a falsetto (bitonal voice).

Direct contact of the trachea with the esophagus often causes their joint damage in some pathological conditions, and then the symptoms of esophageal damage come to the fore. In this case, they speak of tracheoesophageal syndrome, which is characterized by signs of esophageal obstruction and respiratory obstruction of the trachea.

Some pathological conditions of the middle section of the trachea are accompanied by painful sensations that differ from a burning sensation and tickling in that they can radiate in ascending and descending directions, as well as to the spine. Usually, such signs are characteristic of destructive processes (malignant tumors, infectious granulomas, wedged IT), and in such conditions, respiratory tracheal noises are observed - from "white" to tonal whistling.

Esophageal-tracheal fistulas cause the most distressing symptoms caused by the entry of liquid and food masses into the trachea: severe respiratory obstruction, uncontrollable cough, especially if the foreign object reaches the carina.

Low tracheal syndromes are characterized by symptoms similar to those of bronchial lesions. In most cases, this syndrome is characterized by a soreness in the chest in the area of the xiphoid process, the occurrence of a "deep" cough, especially uncontrollable and painful when the pathological process spreads to the tracheal carina.

The diagnosis of the above syndromes is supplemented by methods of X-ray and tracheobronchoscopic examination.

The latter is used for protracted syndromic symptoms that are not characteristic of a banal inflammatory process and are accompanied by an unusual pain syndrome, alarming changes in red blood, bloody or hemorrhagic sputum, etc.

Bronchial syndrome. The manifestations of this syndrome include disorders of bronchial patency, secretory function of their glandular apparatus and sensory disorders that provoke the following symptoms.

Cough is the earliest and most constant symptom of bronchial damage. It is a reflex act that plays a major role in the self-cleaning of the respiratory tract from both foreign bodies and endogenously formed products of various pathological processes (mucus, blood, pus, products of lung tissue decay). This reflex is caused by irritation of the sensory nerve endings of the vagus nerve, from where it is transmitted to the cough center located in the medulla oblongata. Cortical influences on the cough reflex are reduced to the possibility of its manifestation with moderate irritation of peripheral sensory receptors, however, with uncontrollable and strong cough, these influences are insufficient to completely suppress the latter. Cough can be dry, wet, convulsive, bitonal, allergic in origin, cardiac, with diseases of the pharynx, larynx, trachea and bronchi, reflex - with irritation of the endings of the vagus nerve of various (non-respiratory) organs. An example of the latter is "ear" cough, which occurs with irritation of the ear branch of the vagus nerve, "stomach" and "intestinal" cough. The so-called nervous cough is most often a habit that remains for the rest of life.

Sputum is a pathological secretion released from the respiratory tract with coughing.

The amount of sputum secreted per day ranges from 2-3 spittings (in acute bronchitis, in the initial stage of pneumonia) to 1-2 liters (in bronchiectasis, pulmonary edema, etc.).

Usually, sputum is odorless, but when it stagnates and putrefactive bacteria enter it, the sputum becomes foul-smelling (putrefactive bronchitis, bronchiectasis, gangrene of the lung, malignant tumor with decay).

The color, transparency and consistency of sputum depend on its composition or on the accidental admixture of food or inhaled substances (coal dust, paint dust particles, etc.). Sputum can be watery and transparent, viscous and glassy, cloudy, yellow-green, gray, with streaks or clots of blood, homogeneously colored with blood, etc. Sputum is especially viscous in lobar pneumonia, during an attack of bronchial asthma, at the initial stage of banal inflammatory processes in the respiratory tract.

The stratification of sputum is determined by collecting it in sufficient quantity in a transparent glass vessel. In some diseases accompanied by the release of a large amount of sputum (putrefactive bronchitis, bronchiectasis, gangrene of the lung, malignant tumor with decay, sometimes tuberculosis of the lungs with the presence of caverns), sputum is divided into 3 layers when standing. The upper layer is opaque, whitish or greenish, sometimes foamy - consists of purulent fractions, a large amount of mucus and small air bubbles. The middle layer is grayish in color, more transparent liquid. The lower layer is greenish-yellow, loose, flocculent, consisting of detritus and purulent bodies.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ]