Laryngeal tuberculosis: causes, symptoms, diagnosis, treatment

Laryngeal tuberculosis (laryngeal consumption, respiratory tuberculosis) is a chronic infectious disease caused by Mycobacterium tuberculosis, developing, as a rule, against the background of widespread tuberculosis of the respiratory organs, hematogenous (lymphogenous) disseminated process of extrapulmonary localization, or by contact (sputogenous). Characterized by the development of cellular allergy, specific granulomas and a polymorphic clinical picture.

Tuberculosis has been known since ancient times. According to published data, pathological changes in the bones of the spine, characteristic of tuberculosis, were found on a skeleton during excavations near Heidelberg; the age of the find is attributed to the early period of the Stone Age (5000 years BC). Among 10 skeletons of Egyptian mummies, attributed to the 27th century BC, caries of the spine was found in four. As V.L. Einie writes, pulmonary tuberculosis was probably not discovered during excavations because in ancient times the entrails, with the exception of the heart, were buried separately. The first convincing descriptions of the manifestations of pulmonary consumption are found among the ancient peoples of the eastern countries. In ancient Greece, doctors were familiar with the manifestations of tuberculosis, and Isocrates (390 BC) spoke of the contagiousness of this disease. In ancient Rome (1st-2nd centuries AD) Areteus, Galen and others provide a fairly complete description of the symptoms of pulmonary tuberculosis, which prevailed for many subsequent centuries. We find this information in the works of Avicenna, Silvius, Frakastro and other outstanding doctors of the Middle Ages. In Russian medical books of the second half of the 17th century.

Tuberculosis was called "dry disease" and "consumptive sorrow". However, during this period, ideas about tuberculosis were very superficial. Significant advances in the study of tuberculosis were achieved in the 18th-19th centuries in the field of pathological anatomy of this disease, when its main pathomorphological manifestations were discovered, however, although the contagiousness of this disease had already been proven, its causative agent still remained unknown. And so in 1882, the outstanding German bacteriologist, one of the founders of modern microbiology Robert Koch (1843-1910) reported on his discovery of the causative agent of tuberculosis. In his report to the Berlin Physiological Society, the morphology of MBT, methods of their detection, etc. were described in detail. In Russia by the middle of the 19th century, N.I. Pirogov described generalized forms of tuberculosis, acute miliary tuberculosis, tuberculosis of the lungs, bones and joints.

A milestone of great importance was the discovery of anti-tuberculosis prophylactic vaccination by the French scientist C. Guerin in 1921-1926 by introducing a weakened culture of bovine MBT (BCG vaccine). A major role in the diagnosis of tuberculosis was played by the works of the prominent Austrian pathologist and pediatrician K. Pirquet, who discovered a diagnostic skin test for tuberculosis (tuberculin diagnostics) in 1907. The aforementioned works, along with the discovery of "X-rays" in 1895 by the great German physicist W.K. Roentgen, made it possible to clinically differentiate changes in organs, primarily in the lungs, gastrointestinal tract and bones. However, advances in diagnostics and other areas of the tuberculosis problem throughout the 19th century were hampered by the lack of etiological treatment. During the 19th century, and even in its second half, the doctor had mainly hygienic and dietary methods of treating tuberculosis infection. The principles of sanatorium-resort treatment were developed abroad (H. Brehmer) and in Russia (V.A. Manassein, G.A. Zakharyin, V.A. Vorobyov, etc.).

The basis for the newest direction of antibiotic therapy of tuberculosis was the theoretical considerations of I.I. Mechnikov on the antagonism of microorganisms. In 1943-1944, S. Vaksman, A. Schtz and E. Bugie discovered streptomycin, a powerful anti-tuberculosis antibiotic. Later, chemotherapeutic anti-tuberculosis drugs such as PAS, isoniazid, ftivazid, etc. were synthesized. The surgical direction in the treatment of tuberculosis also developed.

ICD-10 code

A15.5 Tuberculosis of the larynx, trachea and bronchi, confirmed bacteriologically and histologically.

Epidemiology of laryngeal tuberculosis

Approximately 1/3 of the world's population is infected with Mycobacterium tuberculosis. Over the past 5 years, the number of newly diagnosed patients with respiratory tuberculosis has increased by 52.1%, and the mortality rate among them has increased by 2.6 times. The most common complication of pulmonary tuberculosis is the development of laryngeal tuberculosis. It accounts for 50% of patients with pulmonary pathology, while tuberculosis of the oropharynx, nose and ear accounts for 1 to 3%. The low percentage of tuberculous lesions of the oropharynx and nose is explained by both the peculiarities of the histological structure of the mucous membrane of these organs and the bactericidal properties of the secretion secreted by the mucous glands.

The main source of infection is a patient with tuberculosis, releasing mycobacteria into the environment, as well as cattle with tuberculosis. The main routes of infection are considered to be airborne, airborne dust, less often - alimentary, hematogenous, lymphogenous and contact.

The risk of developing tuberculosis is high in:

• persons without a fixed abode (homeless people, refugees, immigrants);
• persons released from places of deprivation of liberty
• patients of drug treatment and psychiatric institutions;
• persons in professions associated with direct close communication with people;
• patients with various concomitant diseases (diabetes mellitus, gastric ulcer and duodenal ulcer, HIV-infected or AIDS patients);
• persons who have received radiation therapy, long-term treatment with glucocorticoids, who have had exudative pleurisy; women in the postpartum period;
• patients with an adverse heredity: in particular: in the presence of human leukocyte antigen, the risk of developing tuberculosis increases by 1.5-3.5 times.

The peak incidence is at the age of 25-35 years, with a fairly high incidence in the range of 18-55 years. The ratio of men to women among patients with laryngeal tuberculosis is 2.5/1.

Screening

For screening of the disease, tuberculin diagnostics (mass and individual) is used - a diagnostic test to determine the specific sensitization of the body to mycobacterium tuberculosis.

Fluorography for the population must be performed at least once every 2 years.

An endoscopic examination of the ENT organs with mandatory microlaryngoscopy should be performed on all patients with tuberculosis, especially those suffering from open bacillary forms of pulmonary tuberculosis.

Classification of laryngeal tuberculosis

According to the localization and prevalence of the process in the larynx:

• monochordite;
• bichordite;
• damage to the vestibular folds:
• epiglottis lesion;
• interarytenoid space lesion;
• lesion of the laryngeal ventricles;
• arytenoid cartilage damage;
• subglottic space lesion.

According to the phase of the tuberculosis process:

• infiltration;
• ulceration;
• disintegration;
• compaction;
• scarring.

By the presence of bacterial excretion:

• with the isolation of mycobacterium tuberculosis (MBT+);
• without isolating Mycobacterium tuberculosis (MBT-).

Causes of laryngeal tuberculosis

The causative agents of laryngeal tuberculosis are considered to be acid-fast mycobacteria, discovered by R. Koch in 1882. There are several types of mycobacteria tuberculosis (human type, intermediate and bovine). The causative agents of tuberculosis in humans are most often (80-85% of cases) mycobacteria tuberculosis human type. Mycobacteria intermediate and bovine type cause tuberculosis in humans in 10 and 15% of cases, respectively.

Mycobacteria are considered aerobes, but they can also be facultative anaerobes. Mycobacteria are immobile, do not form endospores, conidia, or capsules. They are quite resistant to various environmental factors. Under the influence of antibacterial substances, mycobacteria can acquire drug resistance. Cultures of such mycobacteria are ultra-small (filterable), persist in the body for a long time, and support anti-tuberculosis immunity. In the event of a weakened immune system, the described forms of the pathogen can again become typical and cause activation of the specific tuberculosis process. In addition, other manifestations of mycobacterial variability include the development of resistance to anti-tuberculosis drugs.

Sources of infection. The main one is a sick person, and all of his secretions can serve as a source of infection. The most important is the sputum of a patient with tuberculosis of the lungs and upper respiratory tract, dried into dust and spreading in the atmosphere (Koch-Cornet theory). According to Flügge, the main source of infection is an airborne infection, spread by coughing, talking, sneezing. The source of infection can be cattle: the infection is transmitted through the milk of animals sick with tuberculosis.

The portals of entry for infection in humans can be the skin, mucous membrane and epithelium of the alveoli of the lungs. The site of entry for MBT can be the lymphadenoid tissue of the pharynx, the conjunctiva of the eyes, the mucous membrane of the genitals. Tuberculosis infection spreads by lymphogenous and hematogenous routes, as well as per continuitatem.

Drug resistance of MBT is due to the widespread use of chemotherapeutic drugs. Already in 1961, 60% of MBT strains were resistant to streptomycin, 66% to ftivazid, 32% to PAS. The emergence of resistant forms of MBT is due to more or less prolonged exposure to subbacteriostatic doses of the drug. At present, MBT resistance to the corresponding specific drugs is significantly reduced due to their combined use with synthetic anti-tuberculosis drugs, immunomodulators, vitamin therapy and rationally selected food additives.

Pathogenesis is complex and depends on the variety of conditions in which the pathogen and the organism interact. Infection does not always cause the development of the tuberculosis process. V.A. Manasein attached great importance to the general resistance of the organism in the pathogenesis of tuberculosis. This position attracted the attention of phthisiologists to the study of the reactivity of the organism, allergies and immunity, which deepened knowledge in the theory of tuberculosis and allowed us to assert that, it would seem, the previously fatal disease tuberculosis is curable. The leading role in the occurrence of tuberculosis is played by unfavorable living conditions and also a decrease in the resistance of the organism. There is evidence of a hereditary predisposition to the disease. Primary and secondary periods are distinguished in the development of tuberculosis. Primary tuberculosis is characterized by high tissue sensitivity to MBT and their toxins. During this period, a primary focus (primary affect) may arise at the site of infection, in response to which, due to sensitization of the body, a specific process develops along the lymphatic vessels and in the lymph nodes with the formation of a primary complex, more often in the lungs and intrathoracic lymph nodes. In the process of formation of foci of primary tuberculosis, bacteremia is observed, which can lead to lymphogenous and hematogenous dissemination with the formation of tuberculous foci in various organs - lungs, upper respiratory tract, bones, kidneys, etc. Bacteremia leads to an increase in the immune activity of the body.

According to modern concepts, immunity to tuberculosis depends on the presence of live MBT in the body, as well as on the functions of immunocompetent cells; cellular immunity is the leading link in the formation of resistance to tuberculosis infection.

Pathogenesis of laryngeal tuberculosis

Laryngeal tuberculosis is considered a secondary disease. The most common source of laryngeal damage is the lungs. The routes of laryngeal infection are different: hematogenous, lymphogenous, contact (sputogenous).

The occurrence of laryngeal tuberculosis is associated with a number of unfavorable factors, both general and local. General factors include decreased reactivity of the body. Among the local factors, the topographic and anatomical features of the larynx should be taken into account. Its location is such that sputum from the bronchi and trachea, getting into the larynx, can linger for a long time in the interarytenoid space, laryngeal ventricles, causing maceration of the superficial layer of the mucous membrane of the larynx, loosening and sloughing of the epithelium. Thus, mycobacteria penetrate through damaged (and even intact) epithelium into the closed lymphatic space of the subepithelial layer of the vocal folds and the interarytenoid space and cause a specific tuberculosis process there. In addition, local predisposing factors include chronic inflammatory processes in the larynx.

The development of laryngeal tuberculosis occurs in 3 stages:

• infiltrate formation;
• ulcer formation;
• cartilage damage.

Infiltration leads to thickening of the mucous membrane of the larynx, the appearance of tubercles similar to papillomas, and then a tuberculoma is formed with subsequent ulceration. The addition of a secondary infection is accompanied by the involvement of the perichondrium and cartilage in the process, and can cause the development of laryngeal stenosis.

Primary tuberculosis of the larynx is rare, more often it is a secondary process with primary localization of infection in the lungs with damage to the intrathoracic lymph nodes. Tuberculosis of the larynx is often accompanied by tuberculosis of the trachea and bronchi, tuberculous pleurisy and tuberculosis of other localizations (tuberculosis of the nose, pharynx, palatine tonsils, bone, articular, skin forms of tuberculosis). Secondary tuberculosis of the larynx, along with tuberculosis of the trachea and bronchi, is the most frequent and formidable complication of pulmonary tuberculosis. The incidence of tuberculosis of the larynx and the severity of the clinical course are directly dependent on the duration and form of the disease. According to A. Ruedi, tuberculosis of the larynx occurs in approximately 10% of patients with the initial form of pulmonary tuberculosis, in 30% of individuals with a long course of the process and in 70% of autopsy cases of those who died from pulmonary tuberculosis. Laryngeal tuberculosis is more common in patients with exudative, open and active forms of pulmonary tuberculosis and less common in productive forms. Sometimes, in primary pulmonary tuberculosis or in old inactive, previously unrecognized tuberculosis foci, the first signs of a general tuberculosis infection may be symptoms of laryngeal lesions, which gives rise to an appropriate examination of the patient and the detection of either the primary focus or the activation of a dormant tuberculosis infection. Laryngeal tuberculosis is much more common in men aged 20-40. In women, laryngeal tuberculosis is more common during pregnancy or shortly after childbirth. Children get sick less often, and at the age of under 10 - very rarely.

Usually, there is a certain parallelism in the clinical course between laryngeal tuberculosis and pulmonary tuberculosis, which is manifested by the same exudative or productive phenomena. However, in a number of cases, such parallelism is not observed: either laryngeal tuberculosis is exacerbated and pulmonary tuberculosis is reduced, or vice versa. In many patients, there is no correspondence between the amount of infected sputum secreted from the pulmonary focus and the frequency or form of tuberculous lesions of the larynx. This fact indicates either the presence or absence of an individual predisposition of a patient with pulmonary tuberculosis to developing laryngeal tuberculosis. Probably, we are talking about the quality of the so-called local immunity, either in an active state or suppressed by some external harmful factors. For example, it has been proven that pulmonary tuberculosis, secondary and primary tuberculosis of the larynx are predominantly suffered by smokers, alcoholics and people whose professions are associated with the presence of harmful agents in the inhaled air that reduce the resistance of the mucous membrane of the upper respiratory tract and lungs to infection.

Infection of the larynx occurs either by an ascending route, in which the infection penetrates the mucous membrane from the sputum secreted from the pulmonary focus, or, much more often, by a hematogenous route. Hematogenous dissemination is observed in closed and miliary forms of tuberculosis. The presence of banal laryngitis contributes to the introduction of MBT into the mucous membrane of the larynx. It has been established that laryngeal lesions are most often located on the same side as the primary focus in the lungs. This is explained by the fact that infection of the larynx occurred by a lymphogenous route from the lymph nodes of the trachea and bronchi on the same side. Another explanation for homolateral laryngeal lesions is the action of the ciliated epithelium, which "delivers" the infection from "its" side to the same side in the larynx. This explanation confirms the canal mechanism of local homolateral damage to the larynx either in the area of the “posterior commissure”, in the interarytenoid space or monolaterally, while with the hematogenous route, foci of tuberculous infection can arise randomly over the entire surface of the larynx, including its vestibule.

Pathological anatomy. From the point of view of the clinical and anatomical classification principle, pathological changes in laryngeal tuberculosis are divided into chronic infiltrative, acute miliary forms and lupus of the larynx. In the chronic infiltrative form, microscopic examination reveals subepithelial infiltrates that transform into diffuse ones, which, spreading to the surface of the mucous membrane and undergoing caseous decay, turn into ulcers surrounded by granulomatous formations, also containing characteristic tuberculous nodules. The mucous membrane appears thickened due to edema and proliferation of the connective tissue membrane. In the productive form of tuberculosis, a fibrosing process with local infiltrates covered with a normal-looking mucous membrane and a slow progressive course predominates. In the exudative form of laryngeal tuberculosis, diffuse ulcers are revealed, covered with gray-dirty deposits and edema of the surrounding tissues. This form of tuberculosis evolves much faster than the productive form, and the spread into the depths of the laryngeal walls and the addition of a secondary infection causes the development of chondroperichondritis and inflammation of the aryepiglottic joints.

In some cases, the epiglottis is destroyed, the remains of which look like a deformed and edematous stump. The edges of the ulcers are raised and surrounded by nodular infiltrates.

The miliary form of laryngeal tuberculosis is much less common than the two above and is characterized by diffusely scattered small nodular infiltrates, red-gray mucosal edema, which cover the entire surface of the laryngeal mucosa and often spread to the mucous membrane of the pharynx. These nodules quickly ulcerate, representing ulcers at different stages of development.

Lupus is a type of laryngeal tuberculosis and microscopically manifests itself by changes similar to the initial pathomorphological manifestations of ordinary laryngeal tuberculosis. Lupus infiltrates are encapsulated and symmetrically located (laryngitis circumscripta), characterized by polymorphism, in which ulcers and even their superficial cicatricial changes, surrounded by dense connective tissue, can be found next to fresh nodular infiltrates. These changes are most often observed along the edge of the epiglottis, the contour of which has the appearance of serrations and is often completely destroyed.

Symptoms of laryngeal tuberculosis

A typical complaint of patients with laryngeal tuberculosis is hoarseness of voice, expressed to varying degrees, and pain in the larynx. When the process is localized in the subglottic space, respiratory failure develops.

Indirect laryngoscopy of the early manifestation of tuberculosis of the vocal folds is characterized by limited mobility of one or both vocal folds, but their complete immobility never occurs. The mucous membrane of the larynx is hyperemic. Hyperemia is caused by subepithelial rashes of tuberculous tubercles. As the process progresses, the number of tubercles increases, and they begin to lift the epithelium, and the hyperemic area of the mucous membrane becomes thickened (infiltrated). Infiltrates ulcerate, erosions and ulcers form on the fold, imitating a "contact ulcer", which acquires a lenticular shape: the bottom acquires a pale gray color.

The tuberculous process in the larynx can also begin with damage to the interarytenoid space. The initial manifestations of tuberculosis in this area, as in cases of damage to the true vocal folds, are represented by limited areas of hyperemia and infiltration with subsequent ulceration, the appearance of a gray-dirty color of the mucous membrane.

The tuberculous lesion in the laryngeal ventricles progresses and spreads to the lower surface of the vestibular fold, and then to the vocal fold. This is the so-called sign of "creeping" of the infiltrate onto the fold. Tuberculous lesions of the vestibular folds are characterized by one-sidedness and partiality of the lesion. The process manifests itself as mild hyperemia of individual areas of the vestibular folds, then slight infiltration of the entire or part of the vestibular fold. In this case, the latter almost completely covers the vocal folds. The process ends with ulceration followed by scarring. Extremely rarely (3% of cases), the tuberculous process affects the subglottic space. In this case, infiltrates are determined that can ulcerate.

Early manifestations of epiglottic tuberculosis: infiltration of the submucosal layer at the junction of the laryngeal and lingual surfaces, or in the area of the border of the epiglottis and vestibular folds. Very rarely, the tuberculous process affects the epiglottis petal and arytenoid cartilages. Consequently, with laryngeal tuberculosis, a mosaic, polymorphic clinical picture occurs.

The tuberculous process in the oropharynx manifests itself as hyperemia, infiltration and ulceration of the anterior (rarely posterior) arches, tonsils, soft palate and uvula. A large number of yellowish-gray nodules-tubercules are determined on the mucous membrane. At the same time, enlarged (to the size of a plum) submandibular lymph nodes, hard in consistency superficial and deep lymph nodes of the neck are palpated.

The tuberculous process in the nose can be localized both in the vestibule of the nose (the inner surface of the wings of the nose), and in the cartilaginous part of the nasal septum, as well as in the area of the anterior ends of the lower and middle nasal conchae. As a rule, one half of the nose is affected. Clinical forms of tuberculosis of the nose: infiltrative-diffuse, limited (tuberculoma), ulcerative (superficial and deep with perichondritis).

Tuberculous otitis is characterized by multiple perforations of the eardrum, which, merging, lead to its rapid disintegration; abundant discharge with a sharp putrid odor. In this case, the bone is often involved in the process, with the formation of sequesters and the development of paresis or paralysis of the facial nerve.

The chronic infiltrative form is more common than other forms. At the initial stage, specific inflammation develops slowly and asymptomatically; the general condition of the patient does not suffer significantly, evening subfebrile temperature may be observed. As the dissemination of MBT from the pulmonary focus of infection progresses, the body temperature rises, chills occur. Gradually, the patient develops a sensation of a foreign body in the throat, increasing pain during phonation, and by the evening - hoarseness of the voice, which soon becomes constant and steadily increases. The patient is bothered by a constant dry cough, caused by both the sensation of a foreign body in the larynx and the developing pathological process in it and in the lungs. Often these phenomena are ignored by both the patient and the attending physician, since the initial morphological changes in the larynx are very similar to an exacerbation of chronic catarrhal laryngitis observed in the patient for a long time. However, atypical for exacerbation of chronic catarrhal laryngitis is the progression of the severity of aphonia, which soon becomes very pronounced, up to complete aphonia. The appearance of ulcers on the epiglottis, aryepiglottic folds, perichondritis of the arytenoid and cricoid cartilages complements the patient's complaints of difficulty and pain when swallowing. Swallowing movements are also accompanied by irradiation of pain to the ear, corresponding to the side of the larynx lesion. Often, even swallowing saliva causes excruciating pain, and patients refuse food, which is why they very quickly develop cachexia. Impaired locking function of the larynx due to damage to the epiglottis and muscles that bring the arytenoid cartilages together, leads to fluid entering the lower respiratory tract and the development of bronchopneumonia. Respiratory failure due to the gradual development of stenosis and the body's adaptation to gradually increasing hypoxia occurs only with extreme stenosis of the larynx, but dyspnea and tachycardia during physical exertion also occur with moderate stenosis of the larynx. Progression of laryngeal stenosis is an indication for preventive tracheotomy, since obstructive phenomena can suddenly reach a critical state, in which tracheotomy must be done in great haste without thorough preparation for it.

The endoscopic picture of the larynx in this form of tuberculosis varies depending on the localization and prevalence of the lesion, which in turn depend on the form of tuberculosis - exudative or productive. In the initial stage, the changes that occur in the larynx are barely noticeable and are difficult to distinguish from the manifestations of banal laryngitis. An indirect sign of laryngeal tuberculosis may be the pallor of the mucous membrane of the soft palate and the vestibule of the larynx, and in the inter-arytenoid space one can notice a papillary infiltration similar to pachydermia. It is this infiltration that prevents the vocal processes of the arytenoid cartilages from fully converging, causing dysphonia.

Another place of frequent development of the tuberculosis process are the vocal folds, on one of which a specific monochorditis develops, which is not particularly difficult to detect. The affected vocal fold appears swollen with a thickened free edge. Such a frequently encountered monolateral localization of tuberculosis infection can exist for a long time, even during the entire main tuberculosis process up to and including its completion, while the opposite fold can remain practically in a normal state.

Further development of laryngeal tuberculosis is determined by the dynamics of the clinical course of the main tuberculosis process. As it progresses and the body's protective properties decrease, the specific inflammatory process in the larynx also progresses: infiltrates increase in size and ulcerate, the edges of the vocal folds acquire a jagged appearance. During indirect laryngoscopy, only part of the ulcer is visible in the interarytenoid space, surrounded by irregularly shaped infiltrates resembling a thickened cockscomb. Similar infiltrative phenomena are observed on the vocal fold, in the subglottic space, and less often on the epiglottis. The latter has the appearance of a thickened immobile shaft covered with ulcers and grape-like infiltrates covering the vestibule of the larynx. Sometimes, reddish-gray edema of the epiglottis hides these changes. The above changes are characteristic of the exudative form of laryngeal tuberculosis, while the productive form is manifested by limited lesions of the circumscripta type, protruding into the lumen of the larynx in the form of a single tuberculoma. The severity of the impairment of vocal fold mobility depends on the degree of damage to the internal muscles of the larynx, secondary arthritis of the cricoarytenoid joints, infiltrative and productive phenomena. In rare cases, infiltration of the mucous membrane of the ventricle is observed, which covers the corresponding vocal fold.

With further development of the tuberculous process, the resulting perichondritis affects the entire skeleton of the larynx, infiltrates and purulent-caseous decay of the prelaryngeal tissues appear with the formation of external fistulas, through which the cartilaginous tissue is palpated with a button probe, fragments of sequesters are released. During this period, the patient experiences severe spontaneous pain in the larynx, which sharply increases at night and does not decrease not only under the influence of conventional analgesics, but also morphine, promedol and other opiates. At the same time, the process in the lungs also worsens. The resulting hemoptysis can be not only pulmonary, but also laryngeal. Often, patients die from profuse pulmonary or laryngeal bleeding with erosion of a large artery.

Acute miliary tuberculosis of the larynx occurs hematogenously and is caused by the seeding of the larynx and often the pharynx with MBT. The disease progresses rapidly, the body temperature rises to 39-40°C, the general condition is poor, there is pronounced dysphonia, reaching complete loss of voice function within a few days. At the same time, there is a violation of the swallowing function, accompanied by excruciating pain syndrome, extremely painful paroxysmal cough, salivation, paralysis of the soft palate, and increasing respiratory obstruction.

Laryngoscopy reveals numerous pinhead-sized, grey, scattered miliary rashes surrounded by a pink halo on the pale and edematous mucous membrane. Initially, these rashes are isolated from each other, then merge to form a continuous inflammatory surface and undergo caseous decay, leaving behind superficial ulcers at different stages of development - from fresh rashes to scars. Similar changes occur on the mucous membrane of the pharynx. With this form of laryngeal tuberculosis, adenopathy of the laryngeal lymph nodes also develops, characterized by severe pain syndrome, often with their caseous decay, fistula formation and subsequent calcification and scarring. Several forms of acute miliary tuberculosis of the larynx have been described: acute, hyperacute, subacute.

The hyperacute form is characterized by a very rapid development of the inflammatory process, leading the patient to death within 1-2 weeks. It is characterized by diffuse ulceration of the mucous membrane, abscess formation and development of phlegmon of the larynx, with extremely pronounced pain and obstructive syndrome, severe intoxication, rapid disintegration of the laryngeal cartilage and surrounding tissues, and the occurrence of erosive bleeding. In this form, all existing types of treatment are ineffective. The subacute form evolves slowly, over several months, and is characterized by seeding of the mucous membrane with nodular formations at different stages of development.

Lupus of the larynx is usually a descending process, the primary focus of which is located either in the area of the external nose or in the area of the nasal cavity, nasopharynx and pharynx. According to statistical data from Albrecht, among patients with the above forms of primary lupus, 10% develop lupus of the larynx. Primary lupus of the larynx is rare. The epiglottis and aryepiglottic folds are most often affected by lupus. Men get sick in middle age, women are slightly more often affected.

Peculiarities of clinical manifestations. General intoxication syndrome may be of varying severity. It is based on the proliferation of bacteria, their dissemination and the action of tuberculosis toxin. According to the severity of local changes, it is possible to distinguish limited foci (small forms) of lesions, widespread changes without destruction, including with damage to several organs, a progressive destructive process. In the past, such forms as tuberculous caseous pneumonia, miliary tuberculosis and tuberculous meningitis, as well as generalized forms of tuberculosis with multiple lesions of various organs were often encountered. And although these forms of tuberculosis are much less common in our time, the problem of primary and secondary tuberculosis remains relevant, especially for closed groups.

Secondary tuberculosis is a long-term, wave-like disease, with alternating periods of exacerbation and attenuation. Local manifestations of primary tuberculosis (for example, larynx, bronchi, pharynx and other ENT organs) are detected mainly in unvaccinated children, in children and adolescents with immunosuppressive and immunodeficiency states. In elderly and senile people, symptoms of tuberculosis are observed against the background of signs of age-related changes in various organs and systems (primarily in the upper respiratory tract and bronchopulmonary system), as well as concomitant diseases.

Pregnancy, especially early pregnancy, and the postpartum period negatively affect the clinical course of tuberculosis. However, mothers with tuberculosis give birth to healthy, practically healthy children. They are usually not infected and should be vaccinated with BCG.

Diagnosis of laryngeal tuberculosis

Physical examination

Anamnesis. Particular attention should be paid to:

• the timing of the onset and duration of causeless vocal dysfunction (hoarseness) that does not respond to standard treatment methods:
• contacts with tuberculosis patients, the patient's belonging to risk groups:
• For young people (under 30 years of age), it is necessary to clarify whether they have been vaccinated or revaccinated against tuberculosis:
• the specifics of the profession and occupational hazards, bad habits;
• previous diseases of the larynx and lungs.

Laboratory research

In a clinical blood test, typical changes include moderate leukocytosis with a shift to the left and anemia.

Microscopic examination of sputum with Ziehl-Nielsen staining or fluorescent microscopy are considered the most informative.

Sputum culture on nutrient media is also used. The disadvantages of the culture method include the duration of the study (up to 4-8 weeks). Nevertheless, the method is quite reliable. In some cases, only this method can detect tuberculosis mycobacteria.

Pathomorphological examination of laryngeal biopsies, which identifies epithelioid, giant cells and other elements characteristic of tuberculous inflammation, including foci of caseation.

Bone marrow and lymph node examinations are used.

Instrumental research

To diagnose laryngeal tuberculosis, microlaryngoscopy, microlaryngostroboscopy, bronchoscopy, biopsy, radiography and CT of the larynx and lungs are used.

It is necessary to conduct spirometry and spirography, which allow us to determine the functional state of the lungs and identify the initial manifestations of respiratory failure caused by pathology of the larynx, trachea, and lungs.

Differential diagnosis of laryngeal tuberculosis

Differential diagnostics are carried out with:

• mycosis of the larynx;
• Wegener's granulomatosis;
• sarcoidosis;
• laryngeal cancer;
• syphilitic granulomas;
• lupus of the upper respiratory tract;
• contact ulcer;
• pachydermia;
• scleroma;
• chronic hyperplastic laryngitis.

CT of the larynx is widely used for differential diagnostics. It reveals signs characteristic of laryngeal tuberculosis: bilateral lesions, thickening of the epiglottis, intactness of the epiglottic and parapharyngeal spaces even with extensive lesions of the larynx by the tuberculous process. On the contrary, radiologically, laryngeal cancer is unilateral, infiltrates adjacent areas: destruction of cartilage and extralaryngeal invasion of the tumor, metastasis to regional lymph nodes are often detected. CT data should be confirmed by the results of pathomorphological examination of biopsies on the affected areas of the larynx.

Indications for consultation with other specialists

If there is no effect from the therapy as a result of drug resistance of Mycobacterium tuberculosis, consultations are necessary.

Treatment of laryngeal tuberculosis

Treatment goals for laryngeal tuberculosis

Treatment is aimed at eliminating clinical manifestations and laboratory signs of tuberculosis of the larynx and lungs, regression of radiological signs of a specific process in the larynx and lungs, restoration of vocal and respiratory functions and the ability of patients to work.

Indications for hospitalization

Long-term (more than 3 weeks) hoarseness of voice and sore throat when swallowing liquid and solid food, not responding to standard treatment methods.

The presence of chronic hypertrophic laryngitis, "contact ulcer".

Non-drug treatment of laryngeal tuberculosis

Among non-drug treatment methods, the following are recommended:

• gentle voice mode:
• gentle high-calorie nutrition;
• balneological treatment.

Drug treatment of laryngeal tuberculosis

Treatment is selected individually, taking into account the sensitivity of mycobacteria tuberculosis to chemotherapy drugs. Treatment is carried out in specialized anti-tuberculosis institutions.

Isoniazid, rifampicin, pyrazinamide, ethambutol and streptomycin are considered highly effective drugs. Usually, at least 3 drugs are prescribed, taking into account the sensitivity of mycobacteria to them. For example, isoniazid, rifampicin, ethambutol for a long time (up to 6 months). Systemic therapy is combined with inhalations of anti-tuberculosis drugs (10% isoniazid solution).

Locally, ointment preparations with anesthetic are applied to ulcer surfaces, infiltrates and ulcers are cauterized with a 30-40% silver nitrate solution, a novocaine blockade of the superior laryngeal nerve or an intradermal novocaine blockade according to A.N. Voznesensky, and a vagosympathetic blockade according to A.V. Vishnevsky are performed.

Treatment of patients suffering from laryngeal tuberculosis is carried out in specialized phthisiology clinics, which employ an otolaryngologist specializing in tuberculous lesions of the ENT organs. His task includes primary and systematic ENT examination of all incoming and treated patients and participation in the treatment process. The main goal of "otolaryngological" treatment is to cure the patient of the laryngeal disease (as well as other ENT organs) and prevent superinfection (perichondritis, phlegmon, "malignant" cicatricial process), as well as to take emergency measures in case of asphyxia in acute stenosis of the larynx (tracheotomy).

Treatment is divided into general, aimed at stopping the primary focus of tuberculosis infection with therapeutic means, or eliminating it by extirpating the affected part of the lung tissue, and local, with the help of which they try to reduce or even prevent destructive changes in the larynx and their consequences. As for chronic cicatricial stenosis, depending on its degree, surgical treatment is also used by laryngoplasty methods.

In the treatment of patients with laryngeal tuberculosis, the same medications are used as in the treatment of pulmonary tuberculosis (antibiotic therapy), however, it should be taken into account that the antibiotics used in tuberculosis have only a bacteriostatic, not bactericidal effect, therefore, under unfavorable conditions (immunodeficiency, poor hygienic and climatic conditions, alimentary deficiency, vitamin deficiency, household hazards, etc.), tuberculosis infection may recur. Therefore, the complex of therapeutic agents must necessarily include hygienic and preventive measures aimed at consolidating the achieved therapeutic effect and preventing relapse of the disease. The antibiotics used in the treatment of patients with laryngeal tuberculosis include the above-mentioned Streptomycin, Kanamycin, Rifabutin, Rifamycin, Rifampicin, Cycloserine. Of the drugs of other classes, the following are used: vitamins and vitamin-like agents (Retinol, Ergocalciferol, etc.), glucocorticoids (Hydrocortisone, Dexamethasone, Methylprednisolone), synthetic antibacterial agents (aminosalicylic acid, Isoniazid, Metazid, Opinizid, Ftivazid, etc.), immunomodulators (Glutoxim), macro- and microelements (calcium chloride, Pentavit), secretolytics and stimulants of the motor function of the respiratory tract (Acetylcysteine, Bromhexine), stimulants of hematopoiesis (Butylol, Hydroxocobalamin, Glutoxim, iron gluconate and lactate and other iron-containing drugs, Leukogen, Lenograstim, Methyluracil and other stimulants of "white" blood). When using antibiotics, a combination of streptomycin and phthivazid gives good results, especially in miliary and infiltrative-ulcerative forms of tuberculosis. It should be borne in mind that a number of antibiotics used in the treatment of patients suffering from tuberculosis have an ototoxic effect (Streptomycin, Kanamycin, etc.). Their detrimental effect on the SpO does not occur often, but when it does, it can lead to complete deafness. Usually, the ototoxic effect begins with tinnitus, so at the first appearance of this symptom, antibiotic treatment should be interrupted and the patient should be referred to an ENT specialist. In such cases, B vitamins, drugs that improve microcirculation are prescribed, 3-4 plasmapheresis sessions and dehydration therapy are performed, rheopolyglucin, rheogluman and other detoxifying agents are administered intravenously.

Local treatment is symptomatic (anaesthetic aerosols, mucolytics, menthol oil infusions into the larynx). In some cases of significant proliferative processes, intralaryngeal microsurgical interventions using galvanocautery, diathermocoagulation, and laser microsurgery may be used. In severe pain syndrome with otodynia, some clinics perform transection of the superior laryngeal nerve on the side of the ear to which the pain radiates.

Treatment of lupus of the larynx includes the use of vitamin D2 in combination with calcium preparations according to the method proposed in 1943 by the English phthisiologist K. Charpy: 15 mg of vitamin is prescribed three times a week for 2-3 months, then 15 mg every 2nd week for 3 months - either per os or parenterally. Calcium gluconate is also prescribed daily at 0.5 g parenterally or per os, milk up to 1 l/day. Food should be rich in proteins and carbohydrates; animal fats in the daily diet should not exceed 10 g. The patient should get a lot of vegetables and fruits.

In case of severe infiltrative and ulcerative lesions of the larynx, PAS and streptomycin are added.

Surgical treatment of laryngeal tuberculosis

If laryngeal stenosis develops, tracheostomy is indicated.

Further management

Patients with laryngeal tuberculosis require dispensary observation. Approximate periods of disability for laryngeal tuberculosis: from 10 months and more according to the conclusion of the VTEK (when there is a tendency to recovery), or registration of disability for patients of voice and speech professions.

Forecast

The prognosis depends on the duration of the disease, the severity of the tuberculosis process, concomitant pathology of internal organs and bad habits.

The prognosis for laryngeal tuberculosis depends on many factors: the severity of the pathological process, its form and stage, the timeliness and completeness of treatment, the general condition of the body and, finally, the same factors related to the tuberculosis process in the lungs. In general, in modern "civilized" conditions of medical care, the prognosis for the condition of both the larynx and other foci of tuberculosis infection is favorable. However, in advanced cases, it may be unfavorable for the functions of the larynx (respiratory and voice-forming) and the general condition of the patient (loss of ability to work, disability, cachexia, death).

The prognosis for tuberculous lupus of the larynx is favorable if the overall resistance of the body is high enough. However, local cicatricial complications are not excluded, in which case dilation or microsurgical intervention methods are used. In immunodeficiency states, tuberculous foci may develop in other organs, in which case the prognosis becomes serious or even questionable.

Prevention of laryngeal tuberculosis

Prevention of laryngeal tuberculosis is reduced to prevention of pulmonary tuberculosis. It is customary to distinguish between medical and social prevention.

Specific prevention of tuberculosis is carried out with a dry anti-tuberculosis vaccine for intradermal administration (BCG) and a dry anti-tuberculosis vaccine for gentle primary immunization (BCG-M). Primary vaccination is carried out on the 3rd-7th day of the child's life. Children aged 7-14 years who have a negative reaction to the Mantoux test are subject to revaccination.

The next important point of prevention is considered to be the medical examination of tuberculosis patients, as well as the introduction of new methods of diagnosis and treatment.

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