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Lecture notes, cheat sheets
ENT diseases. Lecture notes: briefly, the most important
Directory / Lecture notes, cheat sheets Table of contents
Lecture No. 1. Study of the ear. Otolaryngological examination. Ear anomalies 1. Examination of the ear. Otolaryngological examination External examination reveals deformity of the auricle, swelling, hyperemia in the area of the mastoid process, discharge from the ear, impaired facial expressions in case of damage to the facial nerve, enlarged lymph nodes in the area of the tragus, mastoid process, below the auricle, postoperative scars, condition of the entrance to the external auditory canal . On palpation, soreness, volume and consistency of tissue in places of inflammation and pathological changes are noted. Otoscopy is performed using a frontal reflector and an ear funnel. The reflector is aimed at the membrane so that the light beam does not change its position when the left eye is closed and opened. To examine the right ear, the ear funnel is gently inserted with the right hand into the initial section of the cartilaginous part of the auditory canal, and the auricle is slightly pulled back with the left hand (with otoscopy of the left ear, vice versa) upwards and backwards in adults, and downwards in young children. This straightens the ear canal and the membrane becomes visible. For better visibility of the membrane, it is advisable for an inexperienced doctor to remove secretions in the ear canal (sulfur, epidermal crusts, dried pus) using an ear cotton holder or Voyachek's attic probe. In the auditory canal, the presence of secretions (pus, blood), swelling of its walls in the cartilaginous or bone part, narrowings are noted. During otoscopy, attention is drawn to the identification points of the tympanic membrane - the handle of the malleus, its short process, the light cone, the anterior and posterior malleus folds. The color of the membrane is noted (normally pearly gray, and with otitis media - a different degree of hyperemia). The position of the membrane is determined (retracted, bulging) and mobility using an optical funnel or an impedance meter. In the presence of perforation, its size, shape, nature of the edges (in chronic otitis media, cicatricial edges) and localization by quadrants (anterosuperior, anteroinferior, posterior superior and posterior inferior) are noted. There are rim and marginal perforations. With the first of them, the membrane tissue is preserved near the tympanic ring, and the second reaches the bone. The color, smell (of rotten cheese with cholesteatoma), consistency, degree of discharge from the middle ear, the state of the mucous membrane of the tympanic cavity during perforations are characterized. With marginal perforations, primarily in the shrapnel part of the membrane, probing is performed using the Voyachek attic probe to determine bone caries and cholesteatoma. After a thorough toilet of the ear canal and tympanic cavity, otoscopy data can be better evaluated. Discharge from the ear is subjected to bacteriological examination in order to determine the pathogen and its sensitivity to antibiotics. 2. Anomalies in the development of the ear Congenital malformations of the auricle are determined visually by cosmetic defects - macrotia (increase in size), microtia (decrease in size) and protrusion of the auricles. These defects are corrected by operations. When the ears are protruding, an oval skin flap is removed from the behind-the-ear fold. During the suturing of the wound, the auricle is pulled up to the edge of the skin of the mastoid process. Macrotia and microtia are eliminated with the help of plastic surgery. Other deformities of the auricle include the ear of the satyr (a conch elongated upwards in the form of a point), Darwin's tubercle (a protrusion on the curl), the ear of the macaque (smoothness of the curls), etc. In the region of the ascending part of the curl, above the tragus, there are congenital fistulas due to non-closure of the first gill slit. A yellow viscous liquid or pus may come from them. When the fistula is blocked, the skin around the fistula becomes inflamed, and cysts may develop. In the surgical treatment of malformations of the external ear, plastic auricle prostheses are sometimes used. Atresia (fusion) of the external auditory canal may be accompanied by underdevelopment of the middle and inner ear in the form of a lack of auditory ossicles, bone fusions of the middle and inner ear with deafness or hearing loss. Atresias are membranous-cartilaginous and bone, partial and complete. 22% of patients do not perceive whispered and colloquial speech or feel it at the auricle, and 30% - at a distance of 1-2 m. Conductive hearing loss is noted at the level of 40-60 dB, with normal bone conduction, with an air-bone interval of 30-40 dB. 80% of individuals have a severe degree of hearing loss, and 14,8% have deafness. The main group consists of patients with II and III degrees of hearing loss, with very severe forms of dysgenesis - with IV degree. With the help of radiography of the temporal bones according to Schüller, Mayer, Stenvers, magnetic resonance imaging and computed tomography, changes in the middle and inner ear are revealed. The most informative is computed tomography, which allows you to identify the structure of the atresia of the auditory canal, the state of the tympanic cavity, auditory ossicles, the number of cochlear coils, etc. A contrast radiography of the auditory tube is performed to determine its patency. Carry out a thorough audio-logical examination. Bilateral hearing loss and deafness in children lead to a violation of the development of speech and mental abilities. The fate of such children directly depends on the possibilities of surgical and deaf-pedagogical correction of hearing and speech, so they need to be operated on earlier, at the age of 3–5 years, and in case of unilateral pathology, after 10–14 years. Surgical treatment consists of creating a stable external auditory canal using the type of radical ear surgery with tympanoplasty, which involves revision of the auditory ossicles, labyrinthine windows, auditory tube, and the creation of a tympanic cavity with a neotympanic membrane. When indicated, any variant of tympanoplasty, stapedoplasty or fenestration of the horizontal semicircular canal is performed. In each case, the operation is individual and complex, so it is advisable to conduct examination and treatment of patients, especially children with ear malformations, hearing loss, in qualified otolaryngology or maxillofacial surgery clinics (auricular plastic surgery). Lecture number 2. Diseases of the outer ear Among inflammatory diseases of the external ear, there are limited and diffuse external otitis media. In the first case, we are talking about a boil, and in the second - about a large group of inflammatory diseases of bacterial, fungal, viral origin or dermatitis, characterized by severe allergic reactions. Diffuse otitis media includes otitis externa, otomycosis, eczema, dermatitis, erysipelas, herpes, and perichondritis of the outer ear. 1. Furuncle of the external auditory canal The furuncle of the external auditory canal is considered limited external otitis, which occurs only in the membranous-cartilaginous part of the auditory canal, where there are hair and sebaceous glands. Etiology, pathogenesis Most often, a staphylococcal infection is introduced into the glands and hair follicles due to skin trauma when picking the ears with nails or various objects, as well as due to the outflow of pus from the middle ear. The furuncle of the ear canal is a manifestation of general furunculosis due to certain diseases (diabetes mellitus, hypovitaminosis). Clinic Characterized by severe pain in the ear, radiating to the eye, teeth, neck, sometimes throughout the head. The pain depends on the pressure of the inflamed infiltrate on the perichondrium, which is closely soldered to the skin and richly supplied with sensitive nerve fibers. The pain is aggravated by movements of the jaw, chewing, touching the tragus and pulling the auricle. In this regard, otoscopy is carried out carefully with a narrow funnel. The furuncle is localized on any wall of the ear canal. Hearing is not changed, but when the ear canal is obstructed, conductive hearing loss occurs. The furuncle can resolve itself by resorption of the infiltrate or, more often, by opening a pustule in the ear canal. Initially, a yellow dot is noted at the top of the pustule, then a purulent core is formed, after which a crater-shaped opening is determined. The tympanic membrane is not changed. Tissue infiltration may extend to the parotid region, the posterior surface of the auricle, and the mastoid region. Often, the lymph nodes are enlarged and painful on palpation in front, below and behind the auricle, depending on the location of the boil. Body temperature is often subfebrile. The average duration of the disease is 7 days. A furuncle on the anterior or lower walls can be complicated by mumps due to the infection passing through the santorini cracks. A recurrent boil may be associated with diabetes, so a urine and blood test is performed for sugar content. Differential diagnosis With severe behind-the-ear lymphadenitis, the furuncle is differentiated from mastoiditis, which is a complication of acute otitis media. Its difference is changes in the tympanic membrane and hearing loss, as well as a characteristic symptom of mastoiditis - the overhang of the posterior bone wall of the auditory canal. The furuncle is localized in the cartilaginous part of the auditory canal. With the introduction of a thin funnel behind the obturating ear canal, the furuncle restores hearing. Sometimes it is possible to differentiate these diseases only by dynamic observation of the patient and by radiography of the temporal bones. Treatment At the onset of the disease, antibacterial drugs are used: penicillin 500 IU 000 times a day intramuscularly or ampicillin, oxacillin, ampiox 6 g 0,5 times a day, erythromycin or tetracycline 4 IU 100 times a day inside. A turunda soaked in 000% boric alcohol is introduced into the ear canal, and after the furuncle is opened, a turunda soaked in a hypertonic solution of sodium chloride and a solution of penicillin in novocaine is introduced. Assign acetylsalicylic acid, analgin. Good results are given by physiotherapeutic methods of treatment: UHF, SHF and UFO. Surgical treatment of a boil is rarely resorted to when infiltration of surrounding tissues is expressed, regional lymphadenitis and a boil are complicated by mumps. The furuncle is opened under local infiltration anesthesia with an eye scalpel in the region of the tip of the rod. Having expanded the incision, the purulent rod is removed and turunda with hypertonic sodium chloride solution is introduced into the ear canal. With recurrent furunculosis, it is advisable to use autohemotherapy, brewer's yeast, general UVI. In some cases, an autovaccine, staphylococcal toxoid is prescribed. 2. Diffuse purulent otitis externa Purulent inflammation of the skin of the ear canal also extends to the bone part of the ear canal, the subcutaneous layer, and often to the eardrum. Etiology, pathogenesis The cause of diffuse otitis is infection of the skin of the ear canal with mechanical, thermal or chemical trauma, purulent otitis media, influenza, diphtheria. Contributes to the introduction of infection maceration of the skin. Metabolic disorders and allergic manifestations in the body favor the development of infection. Clinic Otitis externa occurs in acute and chronic forms. In the acute stage, diffuse hyperemia, infiltration of the walls of the ear canal, pain during otoscopy, and pressure on the tragus are noted. The process is more pronounced in the cartilaginous part, but extends to the bone part and the tympanic membrane, causing a narrowing of the ear canal. Itching, discharge of desquamated epidermis and pus with a putrid odor are noted. With influenza, hemorrhagic vesicles are observed on the walls of the auditory canal, with diphtheria, dirty gray fibrinous plaques are formed with difficulty. In the chronic course of external otitis, the symptoms are less pronounced, but the skin of the ear canal is thickened, the tympanic membrane is infiltrated. Differential diagnosis Differentiate otitis externa with the average after a thorough toilet of the ear. With otitis externa, hearing acuity is not impaired. After exclusion of the furuncle of the external auditory canal, the main attention should be directed to the differential diagnosis of diffuse purulent external otitis media with eczematous, fungal and viral otitis media. To do this, the discharge from the ear is sown on the flora and its sensitivity to antibiotics, a study on fungi. Treatment A diet is prescribed with the exception of spicy and spicy dishes, rich in vitamins. Carry out hyposensitizing therapy. For this purpose, the following drugs can be prescribed: tavegil, diphenhydramine, pipolfen, claritin, as well as calcium preparations. In the acute form of the process, the ear is washed with a warm 3% solution of boric acid, a 0,05% solution of furacilin. With itching, a 2-5% white mercury ointment or 1-2% ointment with yellow mercury oxide, 1% menthol in peach oil is prescribed. Apply lubrication with a 3-5% solution of silver nitrate, 1-2% alcohol solution of brilliant green or methylene blue. A good effect is the use of hydrocortisone emulsion, 1% prednisolone ointment, oxycort, 1% synthomycin emulsion. UHF, microwave and ultraviolet radiation are combined with drug therapy. In the chronic form, staphylococcal toxoid, antiphagin and vaccines are effective. Polymyxin M (0,5-1% ointment or emulsion) is used to suppress Pseudomonas aeruginosa. With persistent, refractory diffuse external otitis media, laser therapy and X-ray therapy are used. To increase the body's resistance, autohemotherapy and multivitamins are prescribed. Antibiotics and sulfonamides are recommended only for deep and chronic pyoderma, taking into account the sensitivity of the microflora to them. 3. Perichondritis of the outer ear Perichondritis of the outer ear is a diffuse inflammation of the perichondrium involving the skin of the outer ear. Etiology, pathogenesis Perichondritis is caused by an infection, most commonly Pseudomonas aeruginosa. Pathogens penetrate during mechanical trauma, plastic surgery of the external auditory canal during radical surgery, thermal trauma (burns, frostbite), ear furuncle, sometimes influenza and tuberculosis. There are purulent and serous perichondritis. Clinic Pain, swelling and hyperemia appear in the area of the auricle, gradually covering its entire surface, with the exception of the lobe, which does not contain cartilage. With suppuration and accumulation of pus between the cartilage and the perichondrium, fluctuations and pain on palpation are noted. Body temperature is elevated. Then the cartilage is melted by a purulent process, dies, and cicatricial deformation of the shell occurs. Serous perichondritis is less violent than purulent. Differential diagnosis Perichondritis is differentiated with erysipelas and hematoma. With erysipelas, hyperemia covers not only the shell, but also its lobe, and also often extends beyond the outer ear. Othematoma occurs more often after injury, is localized in the area of the anterior surface of the upper half of the auricle, has a purple color, is not painful on palpation, and proceeds with normal body temperature. Treatment In the initial stage of the disease, local and general anti-inflammatory treatment is carried out. When Pseudomonas aeruginosa is detected, penicillin is ineffective. Assign polymyxin M (1% ointment or emulsion), inside tetracycline, oletethrin or oxytetracycline 250 IU 000-4 times a day, erythromycin 6 IU 250-000 times a day, streptomycin 4 IU 6 times a day day intramuscularly. The affected part of the shell is smeared with 5% tincture of iodine, 10% lapis. Physiotherapy is carried out in the form of UVI, UHF or microwave. In some chronic cases, X-ray therapy is used. With suppuration, a wide tissue incision is made parallel to the contours of the auricle, the necrotic parts of the cartilage are removed, the abscess cavity is scraped out with a spoon and a swab with antibiotics is injected into it. Dressings are done daily. If the auricle is deformed in the long-term period, plastic surgery is performed. 4. Exostoses of the external auditory canal Exostoses are bone formations resulting from osteodystrophic processes of the temporal bone. Exostoses grow slowly, often asymptomatically in the form of exostoses and hyperostoses. With obturation of the ear canal, tinnitus, hearing loss appear, the process of excretion of sulfur or pus in otitis media is disturbed. Two forms of exostoses are observed - pedunculated and flat. Pedunculated exostoses originate from the outer ring of the bony part of the ear canal. They are diagnosed by otoscopy and radiography, often as an incidental finding. Stem exostoses are easily knocked off with a flat chisel under local infiltration anesthesia endaurally. Relapses are not noted. Flat exostoses often occupy almost the entire length of one of the walls of the auditory canal. Sometimes they form in the region of the tympanic ring, causing thickening of the wall of the tympanic cavity. Flat exostoses are multiple and make otoscopy difficult. The decision to remove them comes with caution, since the operation is traumatic and does not always give positive results. The operation is partially performed behind the ear access. The tissue of exostoses is dense, and their removal with a chisel requires the application of force, which is associated with the possibility of damage to the structures of the middle ear and facial nerve. Lecture number 3. Diseases of the middle ear Diseases of the middle ear represent the most clinically and socially important group. They often affect adults and especially children. The result of these diseases is hearing loss, leading to a decrease in social activity and professional fitness. In addition, diseases of the middle ear can cause intracranial complications that are fatal. The condition for the normal functioning of the ear is good ventilation through the auditory tube, which, in turn, depends on the condition of the upper respiratory tract. There are acute and chronic otitis media, and by the nature of the exudate - serous and purulent. Diseases of the middle ear are rarely primary. In most cases, they develop against the background of inflammatory processes of the upper respiratory tract, especially in the presence of factors contributing to the violation of ear ventilation: adenoids, nasal polyps, curvature of the nasal septum, hypertrophy of the turbinates, sinusitis and other diseases. Inflammation goes through three stages: alterative, exudative and proliferative. Acute otitis media according to the nature of the exudate is divided into mucous, serous, purulent, hemorrhagic and fibrinous. Purulent inflammation always leads to the formation of perforation of the membrane. With purulent otitis, there is a pronounced exudation with a gradual transition of the mucous exudate into serous, and then into purulent. The severity of inflammation, its prevalence and outcome depend on the degree and duration of the dysfunction of the auditory tube, the virulence of microorganisms, the resistance and reactivity of the human body. 1. Acute tubo-otitis Acute tubo-otitis is characterized by a mucous form of the exudative stage of inflammation. Since there is no free exudate in the tympanic cavity, in this pathology of the middle ear, the main role is played by the inflammatory process in the auditory tube, leading to a violation of its functions, with moderate inflammation in the tympanic cavity. Etiology The cause of acute tubootitis is an infection from the upper respiratory tract that spreads to the auditory tube and tympanic cavity. Infection of the auditory tube most often occurs with acute respiratory viral disease, influenza, and in children with scarlet fever, measles, whooping cough, diphtheria and other infections accompanied by catarrh of the upper respiratory tract. The etiological factor is viruses, streptococci, staphylococci. Pathogenesis The mucous membrane of the auditory tube, nasopharynx and respiratory region of the nasal cavity is covered with cylindrical ciliated epithelium containing many mucous glands, and in the region of the nasopharyngeal mouth of the auditory tube contains lymphoid tissue, so inflammation of the upper respiratory tract quickly spreads to the auditory tube and tympanic cavity. As a result of inflammation of the auditory tube, its functions are violated: ventilation, drainage, barofunction and protective. The reasons for the violation of these functions are permanent and temporary. Permanent causes include adenoid vegetations, hypertrophy of the posterior ends of the inferior turbinates, chronic rhinitis, choanal and other polyps, deviated nasal septum, tumors of the nasopharynx, which can close the nasopharyngeal mouth of the auditory tube and interfere with its ventilation function. Temporary causes include acute inflammation of the upper respiratory tract. The cause of tubo-otitis can be sudden changes in atmospheric pressure during the ascent and descent of the aircraft, as well as during the dive and ascent of divers and submariners. Aerootitis in pilots and mareotitis in sailors may have the character of tubo-otitis. An increase in pressure from the outside is worse tolerated, since it is more difficult for air to penetrate into the tympanic cavity through a compressed auditory tube. The functions of the auditory tube with tubo-otitis are impaired due to inflammation of its mucous membrane and constant closure of the walls. In violation of the ventilation of the tympanic cavity and negative pressure, a transudate may appear in it, containing up to 3% of protein and less often fibrin. In acute tubo-otitis caused by an infection, extravasation is not prolonged and pronounced, since an exudative stage of inflammation occurs. The exudate is scanty, mucous in nature, which gives reason to consider acute tubo-otitis as an inflammation of the middle ear with a predominance of the pathology of the auditory tube. There is no free exudate forming the fluid level in the tympanic cavity. A dull color and retraction of the tympanic membrane are noted. Clinic During an acute respiratory viral infection or immediately after, the patient complains of unilateral or bilateral permanent or intermittent hearing loss, tinnitus. Ear congestion may be the result of an uncompensated difference in atmospheric pressure (for example, after flying on an airplane). The retraction of the tympanic membrane is noted, the characteristic features of which are the apparent shortening of the malleus handle, the protrusion of its short process outwards, the deformation or disappearance of the light cone, and more distinct anterior and posterior malleus folds. Hearing is reduced due to changes in the hydrodynamics of the ear lymph. With impedancemetry, negative pressure in the tympanic cavity is determined. With a slight hyperemia of the tympanic membrane, it is permissible to blow out the ear after a thorough anemization of the nasal mucosa. A characteristic of acute tubootitis is the restoration of hearing after blowing out the ear. Sometimes patients themselves note a periodic improvement in hearing when they yawn or blow their nose. Treatment The main attention is paid to the restoration of the ventilation function of the auditory tube. For this, long-acting vasoconstrictor nasal drops (sanorin, naphthyzin, galazolin, tizin, nazivin) are prescribed 3 times a day. Antihistamines (tavegil, suprastin, diazolin) contribute to the reduction of swelling of the mucous membrane. Symptomatic treatment of acute respiratory viral disease is carried out. After careful anemization of the mucous membrane of the inferior turbinates and mouths of the auditory tubes, the ears are blown. Of the physiotherapeutic methods of treatment, UHF and pneumomassage of the tympanic membrane are recommended. With adequate treatment, acute tubo-otitis often resolves within a few days. With a prolonged course, it is necessary to make an x-ray of the paranasal sinuses to exclude acute sinusitis. 2. Acute serous otitis media Acute serous otitis media is characterized by a serous form of exudative inflammation. Etiology The cause of acute serous otitis media is most often an infection of the upper respiratory tract, which enters the tympanic cavity through the auditory tube. This usually happens during an acute respiratory viral infection, influenza and other diseases that occur with inflammation of the respiratory tract. The causative agents of otitis are viruses, staphylococci, streptococci, pneumococci. In children, the causes of otitis are measles, scarlet fever, whooping cough, diphtheria, etc. Serous otitis often has a protracted course, especially in children, which depends on the nature and virulence of the pathogen, the morphofunctional state of the middle ear and the immunobiological resistance of the organism. Pathogenesis The inflammatory process from the upper respiratory tract extends to the mucous membrane of the tube and into the tympanic cavity. The mucous membrane of the auditory tube is infiltrated, the ciliated epithelium partially dies, the inflamed walls close, and its ventilation and drainage functions are disturbed. Negative pressure in the tympanic cavity leads to venous stasis and the appearance of transudate, and then serous exudate. The mucous membrane is infiltrated by lymphocytes. The squamous epithelium metaplasias into a cylindrical epithelium, is replaced by goblet secretory cells, the mucous glands secrete a copious secret. Free fluid appears in the tympanic cavity. This fluid may be mucoserous, serous, or gelatinous with few cells and often sterile. The secret can dissolve or evacuate into the nasopharynx when the function of the auditory tube is normal, but, thick and viscous, it is more often organized into connective tissue scars. The adhesive process leads to persistent hearing loss. Clinic There is a decrease in hearing, noise in the ear, sometimes pain, as well as a feeling of transfusion of fluid in the ear when the position of the head changes. When otoscopy, a yellowish, milky, brownish or bluish color of the eardrum is observed, depending on the color of the translucent fluid. Sometimes the transudate has the form of foamy bubbles formed when air enters through the auditory tube. When it partially fills the tympanic cavity, the fluid level can be seen as a dark gray line. Often, the symptom of translucence of the secret through the tympanic membrane goes unnoticed due to the initially seemingly favorable course of otitis media. Body temperature is normal or subfebrile. Due to retraction or protrusion of the membrane and a decrease in the mobility of the sound-conducting apparatus, conductive hearing loss is noted. In the presence of fluid in the region of the labyrinth windows, bone and tissue conduction deteriorates, and the tonal perception of high frequencies also suffers. With the disappearance of fluid in the tympanic cavity, hearing improves, bone and tissue conductivity is restored. Treatment Treatment consists primarily in the elimination of acute inflammatory phenomena in the upper respiratory tract to normalize the function of the auditory tube and evacuate the pathological secret from the tympanic cavity by the transtubal or transtympanic route. In the absence of a pronounced general reaction of the body, antibiotics and sulfa drugs are not prescribed, since they can contribute to a more sluggish course of the inflammatory process in the ear and thickening of the secret. Vasoconstrictor nose drops are used (sanorin, galazolin, naphthyzin, nazivin, tizin, imidine). You can not use tableted preparations for the common cold such as rhinopront or coldact, containing anticholinergics and reducing mucus secretion, as this also makes the secret more viscous and difficult to remove from the tympanic cavity. It is advisable to lubricate the mouth of the auditory tube with vasoconstrictor agents, and then with astringents (1-2% silver nitrate solution or 2% protargol solution). Proteolytic enzymes (trypsin, chymotrypsin - 1-2 mg per 1 ml of isotonic sodium chloride solution) are introduced into the tympanic cavity through an ear metal catheter through the auditory tube, which help to thin the secretion. To improve the drainage function of the auditory tube, the introduction of glucocorticoids is indicated. In order to prevent the adhesive process, lidase is introduced at a later period. The introduction of proteolytic enzymes and lidase through electrophoresis is quite effective. The development of the adhesive process is prevented by pneumomassage of the tympanic membrane using the ear apparatus or the Siegl funnel. After the elimination of acute rhinitis, the ear is blown through the Politzer or using an ear catheter. Its effectiveness is evaluated using the Luce otoscope. The use of antihistamines (tavegil, suprastin, diazolin, claritin, diphenhydramine), multivitamins, acetylsalicylic acid and symptomatic agents is shown. If the exudate does not resolve, the function of the auditory tube is not restored and the hearing does not improve, then surgical methods are used to evacuate the secret from the tympanic cavity - tympanopuncture, myringotomy (paracentesis) or tympanotomy with secretion suction and the introduction of drugs into the tympanic cavity. Tympanopuncture and myringotomy are performed in the posterior inferior quadrant of the tympanic membrane. Tympanopuncture is resorted to as a single intervention, but sometimes it is repeated. After myringotomy, a Teflon or polyethylene shunt is inserted into the opening of the tympanic membrane, resembling a spool of thread with protruding edges in shape. Shunting of the tympanic cavity can also be carried out with a polyethylene tube 7-8 mm long. Through the shunt, the secret is repeatedly sucked out from the tympanic cavity and medicinal substances are injected into it. The usual paracentesis of the tympanic membrane with suction of the secret is also justified. Prevention Prevention of acute serous otitis media consists in the prevention of acute inflammatory diseases of the upper respiratory tract and surgical sanitation of the ENT organs. Lecture No. 4. Diseases of the middle ear. Acute suppurative otitis media Acute purulent otitis media. Acute suppurative otitis media is a fairly common disease. In adults, it accounts for 25-30% of ear pathology. Acute purulent otitis media occurs even more often in children, especially infants and young children. Etiology An acute inflammatory process in the middle ear is caused by streptococci, all types of staphylococci and pneumococci. In addition, otitis media can be caused by viruses, fungi, Pseudomonas aeruginosa, Proteus, Escherichia coli, etc. Pathogenesis Acute otitis media develops mainly against the background of an acute respiratory viral infection or other infectious disease and is their complication. For its occurrence, general and local predisposing factors are of great importance. A decrease in the overall resistance of the body as a result of hypothermia, hypovitaminosis, overwork and a complex of other factors leads to the development of an acute respiratory viral infection, accompanied by an inflammatory process in various parts of the upper respiratory tract, including the nasopharynx. Inflammatory edema of the pharyngeal mouth of the auditory tube and its mucous membrane disrupts the ventilation of the middle ear. It creates a place of least resistance, since the constant negative pressure in the tympanic cavity contributes to the swelling of the mucous membrane of the tympanic cavity and the cells of the mastoid process. A decrease in local resistance against the background of viremia leads to the development of inflammation in the ear. With influenza, scarlet fever, measles, the causative agents of these diseases are the cause of the inflammatory process in the ear. This route of infection is called hematogenous. A common cause of inflammation of the middle ear is the microflora of the nasopharynx, which enters it through the auditory tube - by the tubal route. With injuries of the tympanic membrane, the infection can be brought transtympanally. In extremely rare cases, acute otitis occurs from the retrograde spread of infection from the cranial cavity or labyrinth. The occurrence of acute otitis is promoted by chronic diseases of the nose and paranasal sinuses, which violate the respiratory and protective functions, adenoids that cover the nasopharyngeal mouths of the auditory tubes. Otitis can occur after various operations in the nasal cavity, ending with tamponade (especially the back), and tonsillectomy. Inflammation of the mucous membrane occurs in all parts of the middle ear - the auditory tube, tympanic cavity and mastoid process, but in the tympanic cavity, mucoid swelling, small cell infiltration and arterial hyperemia are most pronounced. The thickness of the epithelial layer in it increases by 15-20 times. Exudate accumulates in the cavity, which is first serous and then purulent. With influenza otitis exudate is hemorrhagic. Swelling of the epithelium and abundant exudation in violation of the drainage function of the auditory tube lead to the outward protrusion of the tympanic membrane, melting of its walls and perforation with the release of the contents to the outside. Abundant mucopurulent discharge gradually becomes less abundant, acquiring a purulent character. After the cessation of suppuration from the ear, the perforation of the tympanic membrane may heal, but the congestion of the ear still persists for some time. The criterion for recovery is a normal otoscopic picture and restoration of hearing. Clinic Acute otitis media is characterized by rapid development and a pronounced general reaction of the body. Body temperature rises to 38-39 °C. The number of leukocytes in the blood reaches 12 x 109- 15 x 109/ L. In the clinical course of acute otitis media, three stages are distinguished: preperforative, perforative and reparative. The preperforative stage is characterized by pain syndrome. The pain is felt deep in the ear and has a variety of shades (stabbing, shooting, boring, throbbing). Pain occurs as a result of infiltration of the mucous membrane of the tympanic cavity, as well as the accumulation of exudate in it, which is perceived by the branches of the glossopharyngeal and trigeminal nerves. Often it radiates to the teeth, temple, the entire corresponding half of the head and intensifies when swallowing, coughing. The next symptom is ear congestion, noise in it as a result of inflammation and limited mobility of the eardrum and auditory ossicles. Hearing loss is objectively noted according to the type of sound conduction disturbance. Sometimes, with viral otitis, the inner ear also suffers, which is also expressed in a violation of sound perception. There are objective symptoms on otoscopy. First, retraction of the tympanic membrane appears, accompanied by shortening of the light cone, injection of vessels along the handle of the malleus and radial vessels of the membrane. Then the limited hyperemia becomes diffuse, the identification points of the membrane disappear. It protrudes and is often covered with a whitish coating. Sometimes there may be pain on palpation and percussion of the mastoid process, which is due to swelling of its mucous membrane. The perforated stage occurs on the 2-3rd day from the onset of the disease. After the eardrum is perforated, the pain subsides and suppuration appears from the ear. General well-being improves, body temperature decreases. At first, the discharge is abundant, mucopurulent in nature. At first, they can come from the tympanic cavity through the perforation in portions, synchronously with the pulse. The light rays reflected from them during otoscopy create an effect called a pulsating light reflex. The contours of the perforation itself are often not visible. After a few days, the amount of discharge decreases, they become purulent. Suppuration is observed on average 10 days. reparative stage. In the normal course of the disease, suppuration from the ear stops, and the perforation of the tympanic membrane independently scars. All subjective symptoms subside, hyperemia of the tympanic membrane gradually disappears. However, within 5-7 days, retraction of the tympanic membrane and ear congestion are still observed. Hearing loss in the future occurs only periodically. Later, hearing often returns to normal. These phenomena are associated with the gradual restoration of the ventilation function of the auditory tube. Fungal otitis media It is caused mainly by yeast-like fungi of the genus Candida and mold fungi of the genus Aspergillus. The pain syndrome is not expressed, and the patient is worried about ear congestion. On the tympanic membrane, a whitish or cheesy coating, spots of dark brown or black color are visible. Later, a mucopurulent discharge of a dirty gray color, sometimes with a putrid odor, appears in the ear canal. Mycological examination of discharge from the ear helps to clarify the diagnosis. Viral otitis (hemorrhagic) is most often observed with influenza. During otoscopy, red-blue vesicles filled with blood appear on the eardrum and adjacent skin of the ear canal. These vesicles can be a source of bloody discharge in the ear canal in the absence of perforation of the tympanic membrane. Viral otitis can cause an isolated lesion of the attic. Sometimes the ear labyrinth is also affected. Then there are auditory and vestibular disorders. The pain syndrome is expressed to a large extent. Complications Complications include the following: 1) formation of persistent dry perforation of the eardrum; 2) transition to the chronic form of purulent otitis media; 3) development of the adhesive process; 4) the occurrence of purulent mastoiditis, labyrinthitis, meningitis, abscess of the brain, cerebellum, sinus thrombosis and sepsis. Sometimes the disease immediately takes on a sluggish, protracted character with mild general symptoms. Perforation of the tympanic membrane does not occur, and a viscous secret accumulates in the tympanic cavity, which is difficult to eliminate. Often, this is followed by an adhesive process in the tympanic cavity, which leads to adhesive otitis media. Differential diagnosis It is necessary to differentiate acute purulent otitis media most often with external purulent otitis media and furuncle of the ear canal. It is distinguished from these diseases by the presence of a perforated tympanic membrane, suppuration from the middle ear, and conductive hearing loss. With otitis externa, and especially with the furuncle of the ear canal, pain is noted when the auricle is pulled back. X-ray of the temporal bones according to Schüller contributes to the diagnosis of pathology of the middle ear. In all cases of acute purulent otitis media, a bacteriological examination of discharge from the ear is performed. Treatment Treatment of otitis is carried out in accordance with the stage of the clinical course and its form. In the first stage, the pain syndrome is relieved, the drainage and ventilation functions of the auditory tube are improved, as well as anti-inflammatory therapy. Anesthetic drops are instilled into the ear (5% solution of carbolic acid in glycerin or 20% solution of camphor alcohol). Inside prescribed painkillers, antipyretics and sedatives (analgin, amidopyrine, acetylsalicylic acid, phenobarbital). Nasal drops should have a long and pronounced vasoconstrictor effect. For this purpose, sanorin, naphthyzin, galazolin and their analogues are used 3-4 times a day. The use of vasoconstrictor ointments is less preferred. Oil-based drops from herbs without a vasoconstrictor effect (pinosol) can only serve as an additional remedy. Antibacterial therapy begins with the appointment of penicillin antibiotics (benzylpenicillin 500 IU 000 times a day intramuscularly or ampioks 6 g orally 0,5 times a day). At the same time, hyposensitizing agents are used. A half-alcohol compress is shown on the ear at night, and during the day - a warming bandage. In the absence of exudate in the tympanic cavity, UHF therapy can be used. The role of an intra-ear compress is well performed by a gauze turunda introduced into the external auditory canal, moistened with 3% boric alcohol. In the second stage (perforative), anesthetic alcohol drops, compresses and UHF are canceled. Continue antibiotic therapy and hyposensitizing therapy, the use of vasoconstrictor drops in the nose. After bacteriological examination of discharge from the ear, antibiotics are prescribed, to which the pathogen is sensitive. With staphylococcal flora, erythromycin is indicated. If possible, avoid the use of ototoxic antibiotics (streptomycin, aminoglycosides). If fungal otitis is suspected, a smear is taken on the mycelium of fungi. The main task of local treatment is to provide favorable conditions for the outflow of purulent discharge from the tympanic cavity. To do this, dry toilet of the ear is performed 2-3 times a day, followed by the introduction of gauze turunda into the external auditory canal. Turunda can be dry to absorb discharge, but most often it is moistened with antiseptic or antibacterial solutions. For this purpose, a 20% solution of sodium sulfacyl, a 3% solution of hydrogen peroxide, a slightly pink solution of potassium permanganate, a solution of furacillin, and a hydrocortisone emulsion are used. These funds are prescribed to patients and in the form of ear drops. Boric alcohol at the beginning of the second stage of otitis is not recommended, as it often causes irritation of the mucous membrane of the tympanic cavity and severe pain. When inflammation subsides in the tympanic cavity, its use is shown not only as a bactericidal agent, but also to stimulate reparative processes. Some patients do not tolerate boric alcohol. In these cases, you should not use it. Penicillin-novocaine meatotympanic blockade can be used. It consists in introducing 250-000 IU of benzylpenicillin sodium salt dissolved in 500 ml of a 000% solution of novocaine (or a 3% solution of trimecaine) into the behind-the-ear region. With the correct administration of the solution, whitening of the skin of the posterior and upper walls of the external auditory canal is observed. If spontaneous perforation of the eardrum does not occur, the pain in the ear intensifies, the body temperature continues to rise, the protrusion of the membrane increases, then its paracentesis is performed in the posterior lower quadrant with a special spear-shaped paracentesis needle. In the presence of meningismus or other complications of otitis media, urgent paracentesis is performed as an emergency. It is better to perform it after meatotympanic novocaine blockade. Treatment of fungal otitis is carried out with antifungal antibiotics (nystatin or levorin) in combination with topical application of fungicidal preparations of the imidazole group (nitrofungin, canestene or amphotericin B). Influenza perforative otitis is treated according to the general rules. Often the process is limited to damage to the outer layer of the eardrum and the skin of the ear canal. In this case, the bullae are not opened. The skin of the ear canal is lubricated with oxolin ointment. If the inner ear is affected, intensive care is required for acute sensorineural hearing loss and vestibular disorders. In the third stage of otitis media, antibiotics are canceled, the toilet of the ear and the instillation of ear drops are stopped. Hyposensitizing therapy continues. The main attention after the disappearance of perforation is given to the restoration of the ventilation function of the auditory tube. For this purpose, vasoconstrictors continue to be used in the nose, but potent drops are replaced with ointments. Resume UHF therapy. The ear is blown according to Valsalva or Politzer. If adhesions in the tympanic cavity are suspected, pneumomassage of the tympanic membrane and endaural lidase iontophoresis are prescribed. Lecture number 5. Mastoiditis. Adhesive otitis media 1. Mastoiditis Mastoiditis is the most common complication of acute suppurative otitis media. It occurs when inflammation passes from the mucous membrane of the cells (cells) of the mastoid process to the bone tissue with the onset of osteomyelitis. With primary mastoiditis, the pathological process occurs immediately in the mastoid process, without affecting the tympanic cavity. Secondary mastoiditis develops against or after acute suppurative otitis media. Etiology The causative agents of mastoiditis are the same microorganisms that cause the development of acute purulent otitis media. In 52% of cases, a polyflora is sown, consisting of Proteus vulgaris, Pseudomonas aeruginosa and Streptococcus, in 48% - varieties of Staphylococcus aureus. Pathogenesis Mastoiditis in most cases develops at the end of acute otitis media in patients with a pneumatic type of mastoid structure. A number of factors contribute to the transition of the process to the bone. These include: 1) high virulence of the infection; 2) reduced overall resistance of the body due to various chronic diseases (diabetes, nephritis); 3) difficult outflow of exudate from the tympanic cavity; 4) the occurrence of a block of the entrance to the mastoid cave, preventing the outflow of exudate from the antrum; 5) irrational treatment of acute otitis media. In the presence of these unfavorable factors, mucoid swelling of the mucous membrane of the process progresses, small cell infiltration and circulatory disorders, which causes the cells to fill with serous-purulent, purulent or bloody-purulent exudate. Then osteitis occurs - bone bridges between cells are involved in the process. Since the osteoclastic and osteoblastic antagonistic processes run in parallel, their thickening can be observed before the thinning of the partitions between the cells. The destruction of the bone bridges of the mastoid process leads to the formation in it of a common cavity filled with pus. There is an empyema of the process. Sometimes the process of formation of pathological granulations predominates in the cells. The empyema of the appendix does not manifest itself until the pus has made some kind of outflow path for itself. Several ways of outflow of pus can form at the same time. Clinic More often mastoiditis is noted at the end of acute otitis media. It takes a certain amount of time for the bone to break down. Usually 2-3 weeks pass from the onset of acute purulent otitis media, and then, against the background of an improvement in the clinical picture, pain and suppuration from the ear resume again, body temperature rises and general well-being worsens. Hearing is reduced. Sometimes suppuration is absent due to a violation of the outflow of pus from the middle ear. Pain is noted on palpation or percussion of the mastoid process, more often in the region of the antrum and apex. Pastosity of tissues, smoothness of the behind-the-ear fold and protrusion of the auricle anteriorly can be observed, depending on the severity of inflammation in the process and infiltration of soft tissues. During otoscopy, suppuration is observed. The pus becomes thicker and enters the ear canal in portions under pressure (the pulsating light reflex is resumed). After the pus is removed, it again accumulates in large quantities in the ear canal (reservoir symptom). The eardrum is infiltrated and may have a copper-red color. A pathognomonic symptom of mastoiditis is the overhang of the posterior superior wall of the auditory canal in the bony region due to periostitis. In this place, a fistula sometimes forms, through which pus enters the ear canal. To confirm mastoiditis, an x-ray of the temporal bones according to Schüller is performed. On the radiograph, shading of the cells of the mastoid process, thickening or thinning of their bone walls with periostitis, and destruction of the bridges up to the formation of a cavity with empyema of the process can be noted. Sometimes there are cases of latent course of mastoiditis with serous otitis media. With all the uncertainty of symptoms, there is still hearing loss, dull pain in the ear, a feeling of stuffiness in it, and a history of inflammation of the middle ear. The tympanic membrane is discolored and infiltrated, but may even be intact, since the perforation has either not occurred or has already closed. In contrast to the overhang of the posterior wall of the external auditory canal, only the smoothness of the angle between it and the membrane is noted. With sluggish mastoiditis, osteitis often predominates with the growth of granulations, without a pronounced purulent process. Complications Mastoiditis can be complicated by labyrinthitis or various intracranial complications, the most common of which are sigmoid sinus thrombosis and abscess of the cerebellum or temporal lobe of the brain. The infection is spread by contact. There is also peripheral paresis of the facial nerve. Treatment Treatment of mastoiditis is most often surgical. Conservative treatment in the initial stage of mastoiditis corresponds to the active treatment of acute otitis media. Massive antibacterial and anti-inflammatory therapy is combined with frequent toileting of the ear and the introduction of drugs into it. 2. Adhesive otitis media The presence of a transudate or exudate in the tympanic cavity with prolonged dysfunction of the auditory tube leads to an adhesive process with the formation of adhesions and scars that limit the movements of the auditory ossicles, tympanic membrane and labyrinth windows. Such a hyperplastic reaction of the mucous membrane with its subsequent fibrosis is interpreted as adhesive otitis media. As such, adhesive otitis media is an unfavorable outcome of several ear diseases. Especially often it develops in acute serous otitis, not accompanied by perforation of the eardrum, when viscous mucus cannot drain independently through the auditory tube and creates the so-called sticky ear. A long delay in the recovery of the function of the auditory tube in acute purulent otitis media after spontaneous closure of the perforation of the tympanic membrane also contributes to the organization of the remnants of inflammatory exudate into scar tissue. Acute serous otitis media with inadequate treatment can also turn into an adhesive process. Exudate in chronic purulent otitis media, as a rule, eventually leads to the formation of scars and adhesions in the tympanic cavity, especially in the attic region, sometimes completely delimiting it from the mesotympanum. Adhesive otitis is divided into perforative and non-perforative. Pathogenesis When the pressure in the tympanic cavity is reduced for a long time, the mucous membrane swells and is infiltrated by lymphocytes with the formation of mature connective tissue. Inflammatory exudate or transudate is organized into fibrous bands. This leads to the formation of adhesions, adhesions, calcifications and ossifications in the middle ear cavity. Hyalinization of the mucous membrane surrounding the auditory ossicles, as well as adhesions between the tympanic membrane, auditory ossicles and the medial wall of the cavity, lead to the restriction or complete immobility of the sound-conducting system of the middle ear. A pronounced adhesive process with the overgrowth of the attic, the development of scar tissue in the region of the labyrinthine windows, leading to ankylosis of the stirrup and immobility of the round window, is called tympanosclerosis. Tympanosclerosis is a lesion of the subepithelial layer, which is expressed in hyaline degeneration of the connective tissue. Permanent signs of this tissue are degeneration of the mucous membrane and bone, as well as calcification. There are two types of tympanosclerosis: 1) sclerosing mucositis; 2) osteoclastic mucoperiostitis. After removal of foci of tympanosclerosis, granulations and scars often form in their place. A third of patients who have had chronic inflammation of the middle ear have tympanosclerotic plaques in the tympanic cavity. They are usually localized in areas of narrow spaces with insufficient aeration and a more pronounced inflammatory reaction (in the region of the entrance to the cave, vestibule window, on the auditory ossicles, especially the stirrup). Clinic Adhesive otitis media is characterized by persistent progressive hearing loss, sometimes with low-frequency tinnitus. Otoscopy reveals a dull, thickened, deformed or atrophied tympanic membrane in some areas with retractions, lime deposits and thin mobile scars without a fibrous layer. There are adhesive otitis media with an almost normal otoscopic picture and severe hearing loss after serous otitis media and tubo-otitis media. Typical limitation of the mobility of the tympanic membrane during the study using a pneumatic funnel Sigle. Blowing out the ears does not give a noticeable improvement in hearing. The ventilation function of the auditory tubes is often disturbed. Hearing is reduced according to the mixed type with a predominant violation of sound conduction. The deterioration of bone conduction is facilitated by the limitation of the mobility of both labyrinthine windows and the degeneration of auditory receptors with a long course of the disease. Gellet's experience with ankylosis of the stapes can be negative, as with otosclerosis, and in other cases of adhesive otitis it is inconclusive. Using impedance audiometry, low pressure in the tympanic cavity, limited mobility of the tympanic membrane (tympanogram type B) or, in case of extensive scars, its hyper-compliance (tympanogram type D) are determined. The acoustic reflex of the stirrup is not recorded. With the help of contrast radiography of the auditory tube, a violation of its patency is determined. Treatment First of all, the causes that caused the violation and prevent the restoration of the function of the auditory tube are eliminated. Then the function of the auditory tube is restored by blowing, introducing various medicinal substances into it (lidase, hydrocortisone emulsion, trypsin), UHF therapy, topical application of vasoconstrictor drugs in the nose and oral administration of hyposensitizing agents. In the presence of a helium-neon laser, the walls of the auditory tube are irradiated by means of a light guide inserted into the ear catheter. In order to increase the elasticity of adhesions and reduce their number, lidase (0,1 g of dry matter diluted in 1 ml of a 0,5% solution of novocaine), chymotrypsin (1 ml at a dilution of 1: 1000), an emulsion of hydrocortisone by tympanopuncture. Lidase can be administered by endaural electrophoresis or behind the ear meatotympanic injection. The introduction of these drugs is combined with vibromassage of the tympanic membrane or its pneumomassage using a Sigle funnel. With adhesive otitis media, tympanosclerosis, in the absence of the effect of conservative treatment, surgical treatment is performed. Prevention Prevention of adhesive otitis media is the timely adequate treatment of inflammatory diseases of the middle ear. Lecture No. 6. Diseases of the inner ear. Labyrinthitis. Otosclerosis 1. Labyrinthitis Labyrinthitis is an inflammatory disease of the inner ear. Most often, the disease is an otogenic complication of otitis media. Other complications, such as meningogenic and hematogenous labyrinthitis, are much less common. Meningogenic labyrinthitis occurs mainly in young children against the background of epidemic cerebrospinal meningitis. Infection from the subarachnoid space to the labyrinth spreads through the cochlear aqueduct or the internal auditory meatus. The inflammation is purulent and develops rapidly, which leads to sudden deafness. Vestibular symptoms may be masked by manifestations of meningitis. They are clearly expressed in a one-sided process. Hematogenous labyrinthitis occurs in various infectious diseases and can be serous, purulent and necrotic. Serous labyrinthitis develops more slowly than purulent meningogenic labyrinthitis. With the serous nature of inflammation, complete inhibition of auditory and vestibular functions is not observed. Purulent and necrotic processes proceed unfavorably in the labyrinth. Necrosis arises from the direct action of toxins and vascular thrombosis. Labyrinthitis in infectious diseases can develop against the background of secondary meningitis as a complication of an infectious disease. In this case, its genesis is extremely difficult to establish. Otogenic labyrinthitis can develop in both acute and chronic suppurative otitis media. Etiology and pathogenesis The causative agents of otogenic labyrinthitis can be all types of polymorphic flora found in the middle ear with otitis media. Labyrinthitis occurs against the background of a decrease in the general and local resistance of the organism with a high virulence of the microflora. In acute purulent otitis media, favorable factors for the development of labyrinthitis are the difficulty in the outflow of discharge from the tympanic cavity and an increase in pressure in it. Under the influence of purulent exudate, the membrane of the round window of the cochlea and the annular ligament of the base of the stirrup swell and become permeable to toxins. A further delay in the evacuation of discharge from the tympanic cavity can lead to melting of the membrane of the round window of the cochlea and the penetration of pus into the perilymphatic space of the labyrinth. Chronic purulent epitympanitis can lead to the destruction of the labyrinth capsule in the protrusion of the lateral semicircular canal with the formation of a fistula in its bone wall. Canal fistula can also occur in patients previously operated on for chronic otitis media with inflammation in the postoperative cavity. A protective granulation wall forms around the fistula. Much less often in chronic purulent otitis media, the fistula of the labyrinth occurs in the region of the promontory and the base of the stirrup. With the progression of chronic otitis media, inflammation passes from the bone capsule of the labyrinth to the membranous labyrinth with the development of diffuse purulent labyrinthitis. Serous inflammation causes an increase in perilymph pressure due to the fact that the endosteum lining the bony labyrinth swells and its dilated vessels become permeable to blood plasma. A small amount of cellular elements appears in the perilymph, mainly lymphocytes, as well as fibrin. The development of serous-fibrinous inflammation sometimes leads to such an increase in intra-labyrinthine pressure that the membrane of the round window of the cochlea ruptures and the infection from the middle ear penetrates into the labyrinth. Purulent exudate consists of leukocytes (mainly neutrophilic). The inflammatory process passes to the membranous labyrinth, leading to the death of auditory and vestibular receptors. Clinic Clinical manifestations of otogenic labyrinthitis consist of symptoms of impaired auditory and vestibular functions and depend on its clinical form. Allocate limited, induced, diffuse serous and diffuse purulent labyrinthitis. Limited labyrinth. The first symptom of a limited labyrinthitis before the formation of a labyrinth fistula is dizziness that occurs when the head turns sharply and the body tilts. In such patients, laying nystagmus may be detected. Hearing loss cannot be entirely attributed to labyrinthitis, since chronic suppurative otitis media in itself causes a pronounced mixed hearing loss. Limited labyrinthitis is manifested by pressor nystagmus towards the affected ear from the moment of formation of the fistula of the lateral semicircular canal. It is detected by a tragus test or by touching the fistula with a probe with cotton wool during the toilet of the ear and may be accompanied by dizziness, nausea. Sometimes the fistula, covered with granulations, is found only during the operation, and in the preoperative period, pressor nystagmus cannot be detected. Pressor nystagmus is absent in the fistula of the promontorium or foot plate of the stapes. induced labyrinthitis. With this form, the symptoms of irritation of the labyrinth are manifested in spontaneous nystagmus towards the diseased ear, dizziness and pathological autonomic reactions. The appearance of these symptoms is associated with the toxic effect of the products of acute purulent inflammation in the tympanic cavity on the labyrinth through its windows. An inflammatory reaction in the labyrinth itself has not yet been observed. Hearing loss is also explained by toxic influence. The pathogenesis of induced labyrinthitis resembles the development of meningism in children as a result of difficulty in the outflow of pus from the tympanic cavity in acute otitis media. The phenomena of induced labyrinthitis disappear after unloading the tympanic cavity through perforation of the tympanic membrane or paracentesis. If this does not happen, then an inflammatory reaction occurs in the labyrinth. Induced labyrinthitis may occur after radical ear surgery. Serous diffuse labyrinthitis. With serous labyrinthitis, there is a decrease in hearing of a mixed type with a predominant lesion of sound perception. In the initial stage of serous labyrinthitis, irritation of the receptors of the vestibular apparatus is noted, and then their inhibition. Spontaneous nystagmus is directed first to the diseased side, and then to the healthy side. The phenomena of irritation of the labyrinth can be observed for several days. With the timely elimination of the inflammatory process in the middle ear, complete or partial restoration of the auditory and vestibular functions of the labyrinth is possible. Purulent diffuse labyrinthitis is characterized by vivid clinical manifestations. Purulent inflammation in the labyrinth quickly leads to the death of auditory and vestibular receptors. The irritation phase of the labyrinth is short-term and lasts for several hours. During it, hearing deteriorates sharply, and spontaneous nystagmus occurs in the direction of the diseased ear. Severe dizziness, nausea and vomiting are noted. Patients take a horizontal position. In the labyrinth suppression phase, nystagmus changes its direction towards the healthy ear. There is a harmonious reaction of deflection of the hands and overshooting with both hands towards the slow component of nystagmus. When the intensity of nystagmus decreases, the patient can already get up. When standing and walking, it also deviates towards the slow component of nystagmus. A characteristic sign of labyrinth ataxia is a change in the direction of deviation of the body with the head turned to the side. After the acute purulent process subsides, a sluggish diffuse labyrinthitis can be observed. With a favorable outcome of the disease, the labyrinth later grows into granulations with transformation into fibrous and bone tissues. With an unfavorable course of purulent labyrinthitis, labyrinthogenic purulent meningitis or a brain abscess may develop. The death of the labyrinth is evidenced by the lack of perception of a cry with the muffling of the opposite ear with Barani's ratchet, as well as a negative result of a qualitative caloric test, which is carried out after the elimination of inflammation in the labyrinth and the tympanic cavity. Body temperature is subfebrile and even normal. Treatment With labyrinthitis, complex treatment is carried out. Since otogenic labyrinthitis is a complication of acute or chronic suppurative otitis media, the purulent focus in the middle ear is eliminated first. The unloading operation for acute otitis media is paracentesis of the tympanic membrane, and for chronic otitis media, radical ear surgery. In the presence of mastoiditis, a mastoid operation is performed. Assign dehydration, antibacterial and detoxification agents. Antibiotics are administered in large doses, with purulent labyrinthitis - intravenously. The indication for labyrinthotomy is a labyrinthogenic abscess of the cerebellum. In this case, the causative focus is removed and access to the abscess, which usually lies near the labyrinth, is facilitated. Prevention Prevention of otogenic labyrinthitis is timely diagnosis and rational treatment of purulent diseases of the middle ear. In the presence of a fistula of the labyrinth, timely surgical intervention contributes to the preservation of hearing and the prevention of the transition of a limited labyrinth to a diffuse one. In the presence of labyrinthine symptoms, patients with acute purulent otitis media and exacerbation of chronic otitis need urgent referral to a hospital. 2. Otosclerosis Otosclerosis is a kind of dystrophic ear disease that affects mainly the bone capsule of the labyrinth, manifested by ankylosis of the stirrup and progressive hearing loss. Etiology and pathogenesis It is believed that the disease is inherited in an autosomal dominant manner. Otosclerotic foci are found in 40% of individuals who are carriers of various genetic defects. There is also an opinion that otosclerosis is an anomaly of the constitution, manifested in the inferiority of the mesenchyme of the body. Many believe that the development of otosclerosis is associated with metabolic disorders, which are based on dysfunction of the endocrine glands. Characteristic is the progression of otosclerosis during pregnancy. Although otosclerosis is considered an ear disease, it can cause abnormalities in a number of body systems (bone, vascular, autonomic, endocrine), which manifests itself in the corresponding clinical signs. Changes in the bone labyrinth capsule begin in the medullary spaces. As a result of increased activity of osteoclasts around the blood vessels, the bone tissue decalcifies, and a limited focus of cancellous bone is formed, containing an excessive amount of marrowy spaces rich in blood vessels. This phase of otosclerosis is called active. Subsequently, the newly formed immature spongy bone is resorbed for the second time and, with the help of osteoblasts, turns into a mature lamellar bone. Clinic When examining a patient, attention is paid to the gradual development of the disease, often the bilateral nature of hearing loss, hearing loss in women due to pregnancy, and the presence of otosclerosis in relatives. With otoscopy, atrophy of the skin of the external auditory canals and eardrums is noted due to the thinning of their fibrous layer, a decrease in the sensitivity of the skin of the auditory canals. The ear canals are wide, do not contain sulfur, and are easily vulnerable. Through the atrophic tympanic membrane, the auditory ossicles are clearly visible, and sometimes there is a hyperemic mucous membrane of the promontorium, indicating a pronounced activity of the process. Sometimes there are exostoses of the external auditory canals. In most cases, the eardrum has a normal appearance. Dryness of the skin of the body, brittle nails, excessive vulnerability of blood vessels, blueness of the sclera, pathology of the thyroid and parathyroid glands, pituitary gland, and gonads can be observed. In the anamnesis, brittle bones, rickets, osteomalacia and other pathology of the skeletal system are noted. In a laboratory blood test, a low content of calcium and phosphorus, proteins, and sugar is revealed. A decrease in the activity of cholinesterase in the blood serum testifies in favor of a decrease in the tone of the autonomic nervous system. The content of ACTH increases. Hearing impairment is noted, as a rule, at the age of 16-20 years. A characteristic symptom is tinnitus, often preceded by hearing loss. Hearing loss as a result of ankylosis of the stirrup occurs imperceptibly, progresses over many years. There may be periods of exacerbations, manifested by a sharp deterioration in hearing and increased tinnitus. They occur under the influence of changes in the hormonal sphere in women during pregnancy, childbirth, and difficult experiences. Rarely, an unfavorable form of the disease is observed, characterized by the rapid progression of sensorineural hearing loss. At the beginning of the disease, patients complain of hearing loss in one ear. According to the clinical course, tympanic, mixed and cochlear forms of otosclerosis are distinguished, which are associated with the spread of the otosclerotic process in the ear labyrinth. In the tympanic form of otosclerosis, ankylosis of the foot plate of the stirrup is noted. Hearing is reduced as a violation of sound conduction. The spread of otosclerotic foci to the round window of the cochlea and deep into it leads to the appearance of a sensorineural component of hearing loss, characteristic of a mixed form of otosclerosis. Hearing in this case is reduced by a mixed type. Deterioration of bone conduction can be associated both with impaired mobility of the labyrinth windows, and with the direct effect of otosclerotic foci on the neuro-receptor apparatus of the cochlea. Normal sensitivity to ultrasound is maintained. The cochlear form of otosclerosis is diagnosed with a decrease in tonal hearing, similar to a violation of sound perception. This can be observed as a result of the successive transition of the tympanic form to the mixed form, and then to the cochlear form of otosclerosis with a long course of the disease. Sometimes hearing loss develops quite quickly, masking ankylosis of the stapes, which is associated with increased activity of the otosclerotic process. Treatment Treatment of tympanal and mixed forms of otosclerosis is surgical. Of decisive importance in relation to the expediency of the operation is the state of bone conduction, assessed by the bone-air interval of the tonal audiogram. Good candidates for surgery are those with bone conduction hearing loss up to 15 dB and air conduction hearing loss up to 50 dB. A contraindication to surgical treatment is an active low-quality course of the osteodystrophic process, including "otosclerosis red". Conservative treatment of otosclerosis is indicated to reduce the activity of the otosclerotic process and reduce tinnitus. It is used mainly in the cochlear form of otosclerosis or its unfavorable course. Shown milk-vegetarian diet with salt restriction, rich in vitamins. Calcium and phosphorus preparations are used to compact spongy bone in combination with long-term intake of vitamin D.3. With hormonal disorders, parathyroidin and testosterone are used. Patients with otosclerosis are under the dynamic supervision of a physician. Lecture No. 7. Diseases of the inner ear. Meniere's disease. Sensorineural hearing loss 1. Meniere's disease Meniere's disease is understood as a peripheral labyrinth syndrome of non-inflammatory origin, which develops as a result of a violation of the circulation of the ear lymph. As a rule, the picture of the disease is typical, characterized by bouts of tinnitus, hearing loss, dizziness, ataxia and autonomic disorders (nausea, vomiting, pallor of the skin, cold sweat). In this condition, the patients did not experience convulsions, loss of consciousness, brain diseases, or purulent process in the middle ear. Etiology The etiology of Meniere's disease has not yet been fully understood. Pathogenesis The pathogenesis of the disease is based on a violation of the mechanism of pressure regulation in the lymphatic spaces of the labyrinth. Increased intra-labyrinthine pressure makes it difficult to carry out a sound wave in the fluids of the labyrinth, and also impairs the trophism of labyrinth receptors. Periodically occurring significant increase in pressure is accompanied by a labyrinth crisis due to a sharp inhibition of all sensory cells of the labyrinth. In such a situation, the peripheral labyrinth syndrome of depression naturally manifests itself, characterized by hearing loss and noise in the ear, as well as pathological spontaneous sensory, somatic and autonomic vestibular reactions. Crises in Meniere's disease are more pronounced when one or predominantly one of the labyrinths is affected. Intralabyrinthine pressure may increase for a number of reasons, such as hyperproduction of endolymph by the vascular streak, disruption of its circulation through the endolymphatic ducts, and insufficient resorption in the endolymphatic sac. In addition, intralabyrinthine pressure may increase as a result of increased perilymphatic pressure. In the pathogenesis of an increase in both labyrinthine and intracranial pressure, the vascular factor plays the main role. Its common features are a complex mechanism of regulation of vascular tone by the autonomic nervous system, anomalies and asymmetries in the structure of the cerebral arteries. The asymmetry of the blood supply to the right and left hemispheres of the brain and labyrinths, functionally compensated due to the system of the circle of Willis and collaterals, can manifest itself under various adverse effects: irritation of the sympathetic periarterial nerve plexuses, hypertensive crisis, aggravation of hypotension, psycho-emotional stress. Increased permeability of the vascular wall occurs when there is a violation of water-salt metabolism and various hormonal disorders. The complex structure of the vascular stria, the feeding habits of the receptor cells of the ear labyrinth washed by the endolymph, the specific electrolyte composition of various lymphatic media, the presence of hormone-producing cells in the labyrinth determine its increased vulnerability to various disorders of neuroendocrine and vascular regulation in the body. If these disorders are manifested only by a peripheral labyrinth syndrome without signs of central dissociation and disharmony of pathological vestibular reactions, then in this case we can talk about Meniere's disease. It is unacceptable to attribute any dizziness or ataxia immediately to Meniere's disease. This diagnosis can be established only after a thorough examination of the patient by an otolaryngologist, neuropathologist and therapist in order to exclude a brain tumor, multiple sclerosis, atherosclerosis, vegetative dystonia, hypertension, hypotension, osteochondrosis of the cervical spine, etc. The clinical picture includes the following characteristic features: 1) recurrent nature and paroxysmal course; 2) brevity of attacks; 3) the presence of all signs of peripheral labyrinth syndrome; 4) the presence of signs of labyrinth hydrops and hearing fluctuations; 5) good health in the interictal period (disappearance of vestibular symptoms) with progressive hearing loss; 6) damage mainly to one ear. The disease begins with a gradual hearing loss in one ear, which is not noticed by the patient and is detected only at the time of the first vestibular crisis. Even if a patient turns to an otolaryngologist with complaints of hearing loss, in the absence of vestibular symptoms this is not associated with the onset of Meniere's disease. Patients go to the doctor at the time of a labyrinth attack, which is characterized by tinnitus, hearing loss, dizziness of a systemic nature, spontaneous horizontal-rotary nystagmus in the direction of a better hearing ear, tonic deviation of the hands and overshooting, as well as body deviation in the direction opposite to nystagmus, nausea , vomiting, blanching of the skin and cold sweat. They take a forced horizontal position, close their eyes and try not to make movements that sharply worsen their condition, have little contact and give the impression of detachment from the environment. In the reversible phase of the disease, a fluctuating nature of hearing loss is noted (a slight periodic deterioration or improvement in hearing), which patients rarely pay attention to. Such a fluctuation of hearing occurs due to the instability of increased intralabyrinthine pressure. Hearing in Meniere's disease is initially impaired by the conductive type, and then by the mixed type. Treatment During an attack, patients need emergency care, gentle transportation in the supine position. Strict bed rest is observed. After an attack, the volume of active movements of the head expands gradually. Conservative treatment of Meniere's disease is aimed at stopping the labyrinth crisis and restoring the hydrodynamics of the labyrinth in the immediate period after the crisis. Preventive measures are almost impossible to prevent an attack of Meniere's disease. Relief of the labyrinth crisis is achieved by intramuscular injection of 1 ml of a 2% solution of promedol or a 2,5% solution of aminazine in combination with 0,5-1 ml of a 0,1% solution of atropine sulfate and 1-2 ml of a 1% solution diphenhydramine solution. Promedol is a narcotic analgesic that lowers the summation capacity of the central nervous system and has an anti-shock effect. The neuroleptic chlorpromazine, having a strong sedative effect, reduces spontaneous motor activity, inhibits motor defensive reflexes and, with preserved consciousness, reduces reactivity to endogenous and exogenous stimuli. Atropine is an M-anticholinergic, which has effects opposite to the excitation of parasympathetic nerves, that is, it is a parasympatholytic. Its central cholinomimetic action is manifested in the reduction of muscle tension. The antihistamine drug diphenhydramine relieves spasm of smooth muscles, reduces capillary permeability, prevents the development of tissue edema, and also has a sedative effect, inhibits the conduction of nervous excitation in the autonomic ganglia, and has a central anticholinergic effect. The main directions of further conservative treatment are the elimination of metabolic acidosis, dehydration therapy and improvement of intracranial hemodynamics. An increase in the alkaline reserve of the blood is carried out with the help of intravenous infusions of a 5% solution of sodium bicarbonate. During the first infusion, 50 ml of the solution is administered, and with subsequent infusions, the dose is increased to 150 ml. The course consists of 7 - 10 infusions. Instead of sodium bicarbonate, trisamine buffer can be used. Its maximum dose should not exceed 1,5 g / kg per day. The dehydrating effect is obtained with intravenous administration of 10-20 ml of a 40% glucose solution or intramuscular administration of 1 ml of a 1% solution of furosemide. Glucocorticoids have powerful anti-edematous, anti-shock and stimulating effects. It should be noted that in Meniere's disease, the function of the adrenal cortex is somewhat reduced, therefore, the use of glucocorticoids is not justified. It is advisable to administer 60 mg of prednisolone intravenously, dissolving in 200 ml of isotonic sodium chloride solution. 10 ml of panangin, 5 ml of a 5% solution of ascorbic acid and 3 ml of cocarboxylase can be added to the solution. The microcirculation of cerebral vessels is improved with the help of intravenous injections of various blood substitutes (rheopolyglucin, rheogluman, mannitol, etc.) in the amount of 200-400 ml. At the end of the intravenous infusion of a solution of prednisolone and blood substitutes, 1 ml of furosemide is injected to remove excess fluid from the body. 2. Sensorineural hearing loss Sensorineural (sound-perceiving) hearing loss is understood as a lesion of the auditory system from the receptor to the auditory zone of the cerebral cortex. Depending on the level of pathology, it is divided into receptor, retrocochlear and central (stem, subcortical and cortical). The division is conditional. The most common is receptor hearing loss. Etiology Sensorineural hearing loss is a polyetiological disease. Its main causes are infections, injuries, chronic cerebrovascular insufficiency, noise-vibration factor, neurinoma of the VIII nerve, syphilis, radiation exposure, abnormalities in the development of the inner ear, maternal illness during pregnancy, intoxication with certain medications, salts of heavy metals, phosphorus, arsenic, gasoline; endocrine diseases, alcohol abuse and tobacco smoking. Sensorineural hearing loss may be secondary to diseases that initially cause conductive or mixed hearing loss. Pathogenesis In infectious diseases, ganglion cells, auditory nerve fibers and hair cells are affected. Meningococci and viruses are neurotropic, while other pathogens selectively act on blood vessels, a third are vaso- and neurotropic. Under the influence of infectious agents, the capillary blood supply in the inner ear is disturbed, and the hair cells of the main cochlea are damaged. Serous-fibrinous exudate with lymphocytes, neutrophils, fiber breakdown and connective tissue formation can form around the auditory nerve. The nervous tissue is vulnerable, and within a day, the disintegration of the axial cylinder, myelin and upstream centers begins. Chronic degenerative processes in the nerve trunk lead to proliferation of connective tissue and atrophy of nerve fibers. The basis of deafness and hearing loss in epidemic cerebrospinal meningitis is bilateral purulent labyrinthitis. With mumps, one- or two-sided labyrinthitis quickly develops or the vessels of the inner ear are affected, resulting in hearing loss, deafness with loss of vestibular function. With influenza, a high vaso- and neurotropism of the virus is noted. The infection spreads hematogenously and affects hair cells, blood vessels of the inner ear. More often there is a unilateral pathology. Often develops bullous-hemorrhagic or purulent otitis media. Thus, the pathology of the organ of hearing in infectious diseases is localized mainly in the receptor of the inner ear and the auditory nerve. In 20% of cases, the cause of sensorineural hearing loss is intoxication. Among them, the first place is occupied by ototoxic drugs: antibiotics of the aminoglycoside series (kanamycin, neomycin, monomycin, gentamicin, biomycin, tobramycin, netilmicin, amikacin), streptomycins, cytostatics (endoxan, cisplatin, etc.), analgesics (antirheumatic drugs), antiarrhythmic drugs (quinadine, etc.), tricyclic antidepressants, diuretics (lasix, etc.). Under the influence of ototoxic antibiotics, pathological changes occur in the receptor apparatus. Hair cells are first affected in the main coil of the cochlea, and then along its entire length. Hearing loss develops throughout the frequency spectrum, but more to high sounds. The traumatic origin of hearing loss includes injuries of various origins. The most common causes of damage to the central parts of the auditory system are tumors, chronic cerebrovascular insufficiency, inflammatory processes in the brain, trauma to the skull, etc. Syphilitic hearing loss may initially be characterized by a violation of sound conduction, and then - sound perception due to pathology in the cochlea and the centers of the auditory system. Radicular sensorineural hearing loss is accompanied by neurinoma of the VIII nerve. The progression of conductive and mixed hearing loss often leads to damage to the auditory receptor and the formation of a sensory component, and then the predominance of sensorineural hearing loss. Secondary sensorineural hearing loss in chronic purulent otitis media, adhesive otitis media can develop over time as a result of toxic effects on the inner ear of microorganisms, inflammation products and drugs, as well as age-related changes in the hearing organ. In the cochlear form of otosclerosis, the causes of the sensorineural component of hearing loss are the spread of otosclerotic foci into the scala tympani, the growth of connective tissue in the membranous labyrinth with damage to the hair cells. Clinic Along the course, acute, chronic forms of hearing loss are distinguished, as well as reversible, stable and progressive. Patients complain of constant unilateral or bilateral hearing loss, which occurred acutely or gradually, with progression. Hearing loss can stabilize for a long time. It is often accompanied by subjective high-frequency tinnitus from slight, periodic to constant and painful, sometimes becoming the main concern of the patient. Treatment Distinguish treatment of acute, chronic and progressive sensorineural hearing loss. Initially, treatment should be aimed at addressing the cause of the hearing loss. Treatment of acute sensorineural hearing loss and deafness begins as early as possible, during the period of reversible changes in the nervous tissue - as an emergency. If the cause of acute hearing loss is not established, then it is most often regarded as hearing loss of vascular origin. Recommended intravenous drip of drugs for 8 - 10 days (400 ml of rheopolyglucin, 400 ml of hemodez every other day); immediately after their administration, a drip injection of 0,9% sodium chloride solution (500 ml) is prescribed with the addition of 60 mg of prednisolone, 5 ml of 5% ascorbic acid, 4 ml of solcoseryl, 0,05 cocarboxylase, 10 ml of panangin. Etiotropic agents for toxic sensorineural hearing loss are antidotes: unitiol (5 ml of a 5% solution intramuscularly for 20 days) and sodium thiosulfate (5-10 ml of a 30% solution intravenously 10 times), as well as an activator of tissue respiration - calcium pantothenate (20% solution of 1-2 ml per day subcutaneously, intramuscularly or intravenously). In the treatment of acute and occupational hearing loss, hyperbaric oxygen therapy is used - 10 sessions of 45 minutes each. In a recompression pressure chamber, inhalation of oxygen or carbogen (depending on the spastic or paralytic form of vascular pathology of the brain). Medicines (antibiotics, glucocorticoids, novocaine, dibazol) are administered by behind-the-ear phonophoresis or endaural electrophoresis. During the period of stabilization of hearing loss, patients are under the supervision of an otolaryngologist, they are given courses of preventive maintenance treatment 1-2 times a year. For intravenous drip, cavinton, trental, piracetam are recommended. Then cinnarizine, multivitamins, biostimulants and anticholinesterase drugs are prescribed inside. Symptomatic therapy is carried out. To reduce tinnitus, reflexotherapy is used, a method of introducing anesthetics into biologically active points of the parotid region. Magnetic therapy is carried out with a common solinoid and local or endaural electrical stimulation with a constant pulsed unipolar current. With excruciating tinnitus and the ineffectiveness of conservative treatment, resection of the tympanic plexus is resorted to. With bilateral hearing loss or unilateral hearing loss and deafness in the other ear, which impede speech communication, hearing aids are used. A hearing aid is usually indicated when the average loss of tonal hearing at frequencies of 500, 1000, 2000 and 4000 Hz is 40-80 dB, and conversational speech is perceived at a distance of no more than 1 m from the auricle. Social deafness is considered to be a loss of tonal hearing at a level of 80 dB or more, when a person does not perceive a cry near the auricle and communication among people is impossible. If the hearing aid is ineffective, and communication is difficult or impossible, then the person is taught to contact people with the help of facial expressions and gestures. It is usually used in children. If a child has congenital deafness or it has developed before mastering speech, then he is deaf and mute. Lecture No. 8. Complications of purulent diseases of the middle and inner ear Independent forms of purulent inflammation of the middle ear are acute purulent otitis media, mastoiditis, chronic purulent epitympanitis, mesotympanitis and purulent labyrinthitis. With their unfavorable course, abscesses can develop in neighboring anatomical regions, diffuse inflammation of the meninges (meningitis) and brain matter (encephalitis), as well as a septic state of the body. Etiology The microflora sown from the primary source of infection is mostly mixed and unstable. Nevertheless, coccal flora most often prevails: staphylococci, streptococci, less often pneumococci and diplococci, even less often - Proteus and Pseudomonas aeruginosa. The occurrence of complications and the variant of the development of the inflammatory reaction depend on the virulence of the infection. Pathogenesis The pathogenesis of otogenic complications is complex and ambiguous. In addition to the virulence of the microflora, the state of the general resistance of the organism is of great importance. Ultimately, it is their ratio that determines the direction and severity of the inflammatory response. The more virulent the flora, the more severe the inflammatory process is and the more difficult it is for the body to resist its spread. Therefore, in acute purulent otitis media, otogenic intracranial complications may develop: meningitis, brain abscess, meningoencephalitis, and sepsis. The structural features of the temporal bone and the structures of the middle and inner ear located in it also predetermine the possibility of developing complications. Among them, an abundance of folds and pockets of the mucous membrane of the attic and the cellular structure of the mastoid process are distinguished, ventilation and drainage of which are significantly hampered by inflammation. Complications of acute purulent otitis media are mastoiditis and labyrinthitis. Labyrinthitis can also develop in chronic suppurative otitis media, progressively destroying the temporal bone. The dura mater stands in the way of infection spreading into the cranial cavity, which, along with the blood-brain barrier, is a serious obstacle to the development of intracranial complications. Nevertheless, inflammation, causing an increase in the permeability of the vascular walls, helps to overcome the infection and these barriers, the inflammatory process occurs between the hard and arachnoid membranes of the brain (subdural abscess or limited leptomeningitis), as well as in the cavity of the venous sinuses (sinus thrombosis). Further spread of the infection leads to the formation of an abscess of the temporal lobe of the brain or cerebellum at a depth of up to 2-4 cm. The described process of the spread of infection is called "by continuation." With the generalization of the process due to reduced resistance and altered reactivity of the body, intracranial complications may develop: purulent meningitis, meningoencephalitis or sepsis. The septic condition in acute purulent otitis in children develops hematogenously when bacteria and their toxins enter the blood from the tympanic cavity. Contributing factors are the hyperreactivity of the child's body, the weakness of its protective immune reactions, as well as the difficulty in the outflow of pus from the tympanic cavity. Chronic suppurative otitis media leads to sepsis through sinus thrombosis. The stages of the process are periphlebitis, endophlebitis, parietal thrombosis, complete thrombosis, infection and disintegration of a thrombus, septicemia and septicopyemia. The ways of spreading infection in each of the purulent diseases of the ear are quite specific. Attention should be paid to the fact that the route of infection spread may not be limited to one mechanism (contact, hematogenous, lymphogenous, lymphomarinthogenic). In acute purulent otitis media, the most common route of infection to the cranial cavity is through the roof of the tympanic cavity, predominantly hematogenous. In second place is the path to the labyrinth through the cochlear window and the annular ligament of the vestibule window. Hematogenous spread of infection into the paracarotid plexus and from there to the cavernous sinus, as well as through the lower wall of the tympanic cavity into the bulb of the jugular vein, is possible. With mastoiditis, pus, melting the bone, can break into the behind-the-ear region, through the top of the mastoid process under the muscles of the neck and through its front wall into the external auditory canal. In addition, it is possible for the process to spread into the cranial cavity to the meninges, sigmoid sinus and cerebellum, and through the roof of the antrum to the temporal lobe of the brain. In chronic purulent epitympanitis, in addition to intracranial complications, a fistula of the lateral semicircular canal may form, and labyrinthitis may occur. Sometimes there are associated complications. They are most often sinus thrombosis and cerebellar abscess, as well as meningitis and brain abscess. In this case, it is appropriate to talk about the stages of the spread of infection into the cranial cavity. The main condition conducive to the spread of infection beyond the structures of the middle and inner ear is the difficulty in the outflow of purulent discharge from the tympanic cavity and mastoid cells into the external auditory canal. Clinic In the first place among intracranial otogenic complications is meningitis, in the second - abscesses of the temporal lobe of the brain and cerebellum, in the third - sinus thrombosis. Sepsis develops less frequently. Sinus thrombosis may not be complicated by a septic condition. The most common complication in childhood is diffuse meningoencephalitis. Otogenic diffuse purulent meningitis, or leptomeningitis, is an inflammation of the pia and arachnoid membranes of the brain with the formation of purulent exudate and increased intracranial pressure. As a result of inflammation of the membranes and increased pressure of the cerebrospinal fluid, the inflammatory reaction spreads to the substance of the brain. encephalitis occurs. The general condition of the patient is severe. There is clouding of consciousness, delirium. The patient lies on his back or on his side with his head thrown back. The position lying on your side with your head thrown back and legs bent is called the "pose of a pointing dog." Extension of the head and flexion of the limbs are caused by irritation of the meninges. Body temperature is constantly elevated to 39-40 ° C or more. Pulse quickened. The patient is concerned about severe headache, nausea and vomiting of central origin, associated with increased intracranial pressure. The headache is aggravated by the action of light, sound or touching the patient. The diagnosis is confirmed by meningeal symptoms - neck stiffness, Kernig's symptom, upper and lower Brudzinsky's symptoms, caused by irritation of the posterior roots of the spinal cord. The development of encephalitis is diagnosed when the pyramidal symptoms of Babinsky, Rossolimo, Gordon, Oppenheim appear, indicating damage to the motor centers of the cerebral cortex and anterior horns of the spinal cord. In severe cases, the cranial nerves are affected; the function of the abducens nerve is the first to suffer. Neutrophilic leukocytosis over 20 x 10 is observed in peripheral blood9/l - 25 x 109/l, increased ESR. Purulent meningitis is confirmed by pathological changes in the cerebrospinal fluid. An increase in its pressure is noted (normally it is 150-200 mm of water column, and the cerebrospinal fluid flows out of the needle at a rate of 60 drops per minute). The liquid becomes cloudy, the content of cellular elements increases to tens of thousands per 1 µl (pleocytosis). The protein content increases (norm 150-450 mg / l), the amount of sugar and chlorides decreases (sugar norm 2,5-4,2 mmol / l, chlorides - 118-132 mmol / l). When sowing the cerebrospinal fluid, the growth of microorganisms is detected. Otogenic meningitis, unlike epidemic cerebrospinal meningitis, develops slowly. Sometimes there are fulminant forms of meningitis in acute suppurative otitis media in children. Otogenic abscesses of the temporal lobe of the brain and cerebellum occur in the immediate vicinity of the focus of infection. These abscesses are primary in contrast to deep and contralateral secondary abscesses in sepsis. In the temporal lobe of the brain, the abscess is more often round in shape, and in the cerebellum it is slit-like. Smooth-walled abscesses with a well-defined capsule proceed most favorably. However, the capsule is often absent and the abscess is surrounded by inflamed and softened brain matter. Allocate the initial, latent and explicit stages of abscess development. The initial stage is characterized by mild brain symptoms: headache, weakness, nausea and vomiting, subfebrile body temperature. Its duration is 1-2 weeks. Further, within 2-6 weeks of development of the latent stage, no obvious symptoms of brain damage are observed, but the patient's state of health is more often changed. The mood worsens, apathy develops, general weakness, increased fatigue are noted. The apparent stage lasts an average of 2 weeks. Symptoms in the explicit stage can be divided into four groups: general infectious, cerebral, conductive and focal. The first group includes general weakness, lack of appetite, stool retention, weight loss. Body temperature is usually normal or subfebrile, ESR is increased, leukocytosis is moderate without significant changes in the leukocyte blood count. There may be an occasional irregular increase in body temperature. Cerebral symptoms are characterized by increased intracranial pressure. Headache, vomiting without previous nausea, neck stiffness, Kernig's symptom are characteristic. Unlike meningitis, there is bradycardia due to pressure on the medulla oblongata. Focal neurological symptoms are of the greatest diagnostic value. Damage to the temporal lobe of the brain (left - in right-handers and right - in left-handers) is characterized by sensory and amnestic aphasia. With sensory aphasia and intact hearing, the patient does not understand what is being said to him. His speech becomes a meaningless set of words. This is due to damage to the center of Wernicke in the middle and posterior sections of the superior temporal gyrus. The patient also cannot read (alexia) and write (agraphia). Amnestic aphasia is manifested by the fact that the patient describes their purpose instead of the name of objects, which is associated with visual-auditory dissociation as a result of damage to the lower and posterior parts of the temporal and parietal lobes. Cerebellar abscess is characterized by impaired limb tone, ataxia, spontaneous nystagmus, and cerebellar symptoms. With brain abscesses, moderate neutrophilic leukocytosis is noted with a shift of the leukocyte formula to the left, an increase in ESR up to 20 mm/h and above. CSF flows out under pressure, transparent, with a low protein content and mild pleocytosis (up to 100-200 cells per 1 µl). With a breakthrough of pus into the subarachnoid space, secondary meningitis develops with a corresponding picture of cerebrospinal fluid. The dislocation of brain structures is confirmed by echoencephalography. The exact localization of the abscess is established by means of computed tomography or magnetic resonance imaging. In the absence of the possibility of performing the latter, cerebral angiography and pneumoencephalography, as well as radioisotope scintigraphy, can be performed. otogenic sepsis. Generalization of infection in acute otitis occurs often primary hematogenous, and in chronic otitis media - most often after thrombophlebitis of the sigmoid sinus. Less commonly, the bulb of the jugular vein, transverse, superior and inferior petrosal sinuses are affected. The infection and disintegration of a blood clot leads to the penetration of a purulent infection into the bloodstream. Sinus thrombosis does not always lead to sepsis. Even in the case of infection, its organization is possible. With sinusogenic sepsis, the prognosis in the vast majority of cases is favorable. Mortality is 2-4%. There are three clinical forms of otogenic sepsis: septicemia, septicopyemia and bacterial shock. With the primary hematogenous nature of sepsis on the basis of acute purulent otitis in children, the septic reaction develops rapidly, but it is relatively easily reversible. This form of sepsis is characterized predominantly by septicemia and toxemia. With a pronounced decrease in resistance and a change in reactivity, fulminant forms of sepsis can be observed. Their prognosis is unfavorable. The characteristic symptom of sepsis is hectic remitting fever accompanied by chills followed by profuse sweating. There may be several such sharp rises and falls in temperature during the day, so body temperature is measured every 4 hours. In children, the temperature is often elevated constantly. Pallor of the skin with an earthy tint is noted. Yellowness of the skin and icterus of the sclera develop as a result of disseminated intravascular coagulation (DIC) and hepatosplenomegaly. Blood changes consist in severe neutrophilic leukocytosis with a shift of the leukocyte formula to the left, toxic granularity of neutrophils, an increase in ESR, increasing hypochromic anemia, hypoalbuminemia and hypoproteinemia. Treatment Treatment of otogenic complications involves the urgent elimination of a purulent focus in the ear and brain, as well as intensive drug therapy. An otolaryngologist performs paracentesis of the tympanic membrane in case of acute purulent otitis media, mastoid surgery in case of mastoiditis and radical surgery in case of chronic purulent otitis media and labyrinthitis. Mastoid and radical ear surgeries are performed with exposure of the dura mater of the middle and posterior cranial fossae, as well as the sigmoid sinus. The condition of the dura mater is assessed (presence or absence of an inflammatory reaction, extradural abscess). If a subdural abscess or abscess of the temporal lobe of the brain and cerebellum is suspected, the brain substance is punctured to a depth of 4 cm. The sigmoid sinus is also punctured to diagnose thrombosis. An abscess of the brain tissue is most often opened along the needle, and drains are introduced into the wound. Sanitation can also be carried out in a closed way through punctures and washing the abscess cavity with antiseptic solutions. If there is an abscess capsule, it is removed with the capsule. When a thrombus is detected in the sigmoid sinus, its wall is dissected longitudinally and most of the thrombus is removed. When thrombosis spreads to the internal jugular vein, it is ligated at the level of the middle third of the neck. Intensive care involves the introduction of large doses of antibiotics. After receiving the result of a bacteriological examination of discharge from the ear, brain abscess, blood, cerebrospinal fluid, antibiotics are used in accordance with the sensitivity of the microflora to them. Other areas of intensive care are dehydration and detoxification with diuretics, solutions of various blood substitutes (rheopolyglucin, rheogluman, mannitol, etc.), glucocorticoids. Glucose, ascorbic acid, B vitamins, antihistamines and symptomatic agents can be administered intravenously and intramuscularly. In case of thrombosis of the sigmoid sinus, under the control of the level of prothrombin and the time of blood clotting, anticoagulants are prescribed (heparin, 10 - 000 IU per day). With otogenic sepsis, blood transfusions, transfusions of fresh frozen plasma, extracorporeal ultraviolet irradiation of blood, plasmapheresis, and hemosorption are indicated. Patients with suspected otogenic intracranial complications need urgent hospitalization, and if the diagnosis is confirmed, they are subject to urgent surgical treatment. Timely diagnosis, paracentesis of the tympanic membrane in acute purulent otitis media, as well as dispensary observation of patients with chronic purulent otitis media and early sanitation of the ear are effective measures to prevent otogenic complications. Lecture No. 9. Traumatic damage to the ear According to the factor causing damage, ear injuries can be different. The most common damaging factors are mechanical, chemical and thermal. Injuries are superficial (without destruction of bones) and deep (with cracks and fractures of the temporal bones). 1. Mechanical damage Othematoma - a hemorrhage between the cartilage and the perichondrium of the auricle. The causes of hematomas are injuries of the auricle. Even a mild injury to the auricle can cause hematoma. It looks like a hemispherical smooth swelling of a purple color on the anterior surface of the auricle, it can be painful, fluctuating. Treatment A small hematoma can resolve on its own or after lubricating it with an alcohol solution of iodine and applying a pressure bandage. In the absence of reverse development of the hematoma, it is punctured, the contents are aspirated, a few drops of a 5% alcoholic solution of iodine are introduced, and a pressure bandage is applied. When indicated, the punctures are repeated. If they are unsuccessful, then the hematoma is opened and drained. With suppuration, the development of chondroperichondritis, incisions are made with scraping of granulations, dead tissues, washed with antibiotics, drained and applied with a pressure bandage. Antibiotics are prescribed parenterally, taking into account the sensitivity of the flora to them. In case of cartilage fractures, fragments are set and a modeling pressure bandage is applied. 2. Damage to the auricle Superficial damage to the auricle occurs with bruises, bumps, cuts, insect bites. There is a partial or complete detachment of the auricle. Treatment The skin around the wound is toileted with alcohol, primary cosmetic sutures are applied under local anesthesia, and an aseptic bandage is applied. Tetanus toxoid is injected subcutaneously. Antibiotics are prescribed intramuscularly or sulfa drugs inside. In the absence of suppuration, the wound heals by primary intention. When the wound suppurates, the sutures are removed after a few days and treated according to the rules of purulent surgery (since ancient times, they sound like this: "Where the pus is, open it there"). With deep (stab and incised) wounds, avulsions of the auricles, primary surgical treatment is performed, foreign bodies, non-viable tissues are removed, then the wound is sutured. Novocaine anesthesia is produced with penicillin. 3. Damage to the eardrum Damage to the eardrum occurs as a result of an increase or decrease in pressure in the ear canal due to hermetic closure during a blow to the ear, falling on it, playing snowballs, jumping into the water, violation of the rules of compression and decompression in divers, caisson workers, barotrauma from an explosion, and also in the treatment of patients in a pressure chamber. The integrity of the tympanic membrane can be broken in case of fractures of the base of the skull, the pyramid of the temporal bone. There is a sharp pain in the ear, noise and hearing loss. With otoscopy, hemorrhages in the tympanic membrane, hematoma in the tympanic cavity, bleeding from the ear and traumatic perforation up to a complete defect of the membrane are observed. Treatment In case of bloody discharge in the ear canal, the doctor carefully makes a dry toilet of the ear with the help of a cotton holder or a suction device to view the eardrum. Then a sterile dry turunda is introduced into the ear canal. The introduction of drops into the ear and washing it are strictly contraindicated due to possible infection. Antibiotics are prescribed intramuscularly to prevent otitis media, and if it develops, then treatment is used, as in acute purulent otitis media. Small traumatic perforations are often replaced by scar tissue spontaneously. With large fresh dry perforations, it is advisable to stick an egg amnion (film) on the eardrum, through which, like a bridge, the epithelium and epidermis can regenerate, closing the perforation. 4. Damage to the auditory ossicles Damage to the auditory ossicles can be combined with a violation of the integrity of the tympanic membrane. A fracture of the malleus, anvil, their dislocation, displacement of the plate of the base of the stirrup develop. If otoscopy and microscopy do not reveal damage to the auditory ossicles, then it is difficult to diagnose this (conductive hearing loss depends on the state of the entire circuit of the sound-conducting apparatus). With an intact tympanic membrane, a break in the ossicular chain can be detected using tympanometry when a type D tympanogram (hypercompliance of the tympanic membrane) is detected. With perforation of the tympanic membrane and violation of the auditory ossicles, the nature of their pathology is most often recognized during the operation - tympanoplasty. Treatment Various types of tympanoplasty are performed depending on the nature of the traumatic injuries of the auditory ossicles and the tympanic membrane in order to restore sound conduction in the middle ear. 5. Fracture of the temporal bones There are longitudinal and transverse fractures of the temporal bone. The longitudinal fracture corresponds to the transverse fracture of the base of the skull. With a longitudinal fracture of the pyramid of the temporal bone, there may be a rupture of the tympanic membrane, since the crack passes through the roof of the tympanic cavity, the upper wall of the external auditory canal. There is a serious condition, bleeding and liquorrhea from the ear, hearing loss. There may be facial paralysis. X-ray of the temporal bones confirms a fracture or fissure. Fractures of the base of the skull and the pyramid of the temporal bone in the absence of external wounds, but the outflow of cerebrospinal fluid from the ear are considered open injuries due to the possibility of infection of the cranial cavity. Transverse fracture. With a transverse fracture of the temporal bone, the tympanic membrane often does not suffer, the crack passes through the mass of the inner ear, therefore, auditory and vestibular functions are disturbed, and paralysis of the facial nerve is detected. Bleeding and liquorrhea from the ear does not happen. A particular danger of fractures of the temporal bone is the possible development of intracranial complications (otogenic pachyleptomeningitis and encephalitis) when the infection penetrates from the middle and inner ear into the cranial cavity. Pay attention to the serious condition of the patient, spontaneous vestibular reactions (dizziness, nystagmus, hand deviation, disturbance of static and dynamic balance, nausea and vomiting), a symptom of a double spot on the dressing material during bleeding from the ear with otoliquorrhea, hearing loss or lack of hearing, paralysis of the facial nerve , meningeal and focal cerebral symptoms. Treatment First aid consists in stopping the bleeding from the ear, for which the ear canal is tamponade with sterile turundas or cotton wool, and an aseptic bandage is applied. The patient is transported lying on his back, ensuring immobility. In the hospital, with an increase in intracranial pressure, a lumbar puncture is performed. With heavy bleeding and signs of intracranial complications, a wide surgical intervention is performed on the middle ear. The prognosis for trauma to the temporal bone depends on the nature of the skull base fracture and neurological symptoms. Extensive injuries often lead to death immediately after injury. In the days following the injury, the cause of death is compression of the brain by a hematoma. Recovery is rarely complete. Headache, dizziness, hearing loss or deafness remain, often with epileptiform seizures. 6. Otoliquorrhea Otoliquorrhea usually resolves on its own. With continued liquorrhea, an operation is performed on the middle ear with exposure of the dura mater and plasticity of its defect with the temporal muscle. Persistent facial paralysis requires surgical decompression. The bone canal of the nerve in the temporal bone is exposed, and its epineural sheath is opened. When a nerve is ruptured, the edges are sutured or neuroplasty is performed. The operation should be carried out before the onset of irreversible degenerative changes in the nerve (no later than 6 months from the moment of injury). 7. Foreign bodies of the ear Foreign bodies in the external auditory canal are more common in children who stick various small objects into their ears during games. In adults, foreign bodies may be fragments of matches, pieces of cotton wool stuck in the ear canal. Sometimes in a dream, insects enter the ear. Symptoms depend on the size and nature of foreign bodies in the outer ear. Foreign bodies with a smooth surface do not injure the skin of the ear canal and do not show symptoms for a long time. Other objects often lead to the appearance of otitis externa with a wound and ulcerative surface. One of the symptoms of an obturating foreign body is conductive hearing loss and tinnitus. With partial blockage of the ear canal, hearing does not deteriorate. Insects at the moment of movement in the ear cause unpleasant, painful sensations, especially in the area of the eardrum. With rough, unsuccessful medical manipulations during an attempt to extract a foreign body, damage to the eardrum and middle ear may occur. Recognition of foreign bodies does not cause difficulties in otoscopy and probing. Treatment Free-lying foreign bodies are removed by washing the ear with warm water or a solution of furacillin from a Janet syringe with a capacity of 100-150 ml. In the presence of perforation of the tympanic membrane or purulent otitis, it is recommended to remove it with a Woyachek's bellied probe or a hook. It is not recommended to remove a foreign body with tweezers or forceps in order to avoid pushing it into the depth of the ear canal and damaging the eardrum. Insects are killed by dropping 70-degree alcohol or liquid sterile oil into the ear, then washing them out. Swollen foreign bodies are removed after reducing the volume by instillation of alcohol. When wedged foreign bodies in the ear canal or their introduction into the tympanic cavity, when it is impossible to remove in the usual way, they resort to surgical treatment. Under local or general anesthesia, a behind-the-ear incision of soft tissues is made, separated, the posterior skin wall is dissected, and the foreign body is removed. Lecture No. 10. Diseases of the nose and paranasal sinuses. Injuries of the nose and paranasal sinuses Nose injuries are one of the most common injuries to the human body. The nature of the damage is determined by the magnitude of the acting force, its direction, and the characteristics of the traumatic object. Injured facial tissues are easily infected with the formation of festering hematomas, phlegmon and thrombosis of the venous tract. Gunshot wounds usually cause more serious injuries. They are often accompanied by injury to adjacent areas, requiring the participation of related specialists in the treatment of the injured. 1. Injuries of the nose and paranasal sinuses of a non-gunshot nature Injuries to the nose and paranasal sinuses of a non-gunshot nature can be closed and open. Blunt trauma to the external nose is accompanied by epistaxis, hematoma around the nose and eyes, deformity of the external nose, impaired breathing and smell. In severe cases, damage captures the deep parts of the nose and the bone structures of adjacent areas. Often, with blunt blows, in addition to the bones of the nose, the bone structures of the orbit and its contents are damaged. In these cases, there are combined injuries of the nose. The eyeball is injured to varying degrees. Blunt trauma to the frontal bone leads to a fracture of the anterior wall of the frontal sinus, which is clinically manifested by depression, often corresponding to the type of traumatic object. Damage to the frontal sinuses, especially in the region of the root of the nose and the medial wall of the orbit, may be accompanied by a violation of the integrity and function of the fronto-nasal canal. A strong direct blow applied to the root of the nose can lead to a very severe combined injury, the so-called fronto-basal (or fronto-facial) injury. In these cases, with possible minimal damage to the skin, there are numerous fractures of the bones of the external and internal nose, as well as adjacent bone formations. The external nose may be roughly pressed inwards. A deep fronto-nasal fold is formed. The ethmoid labyrinth is grossly damaged, displaced posteriorly, sometimes to a considerable depth. In this case, the structures of the sphenoid bone can also be injured. Damage to the ethmoid bone and its sieve plate leads to anosmia and the appearance of subcutaneous emphysema on the face, manifested as swelling and crepitus. It is also possible for air to enter the cranial cavity (pneumocephalus). In some cases, these fractures form a valve valve, which causes a dangerous injection of air into the cranial cavity. Fractures in the region of the sphenoid bone may be accompanied by damage to the wall of the internal carotid artery. In the event that death does not occur immediately after injury, an arterial aneurysm is likely to develop, caused by damage to the adventitia. 2-3 weeks after the injury, sudden severe nosebleeds may appear, pouring into the nasopharynx and associated with the dissection of the resulting aneurysm. Clinic In the case of a fracture of the bones of the nose, an external examination determines the deformity of the external nose, expressed to one degree or another. There is swelling and swelling of the soft tissues of the nose and adjacent areas of the face. The hematoma gradually increases, which makes it difficult to assess the magnitude of the deformity and reposition the bones of the nose. Swelling of soft tissues in the nose and on the face can also be caused by subcutaneous emphysema, which, on palpation, is defined as a slight crackling crackle. The latter is a sure evidence of damage to the paranasal sinuses, primarily the ethmoid labyrinth. Palpation with fractures of the nasal bones and cartilage detects osteochondral crepitus. The diagnosis of a fracture of the bones of the nose is confirmed by X-ray examination. Hematoma of the soft tissues of the face is often accompanied by hemorrhage in the area of the eyelids and around the orbit (a symptom of glasses). In these cases, it is necessary to perform an X-ray examination, since this symptom may be the only sign of a fracture of the base of the skull. For specification of the diagnosis the lumbar puncture is shown. The presence of blood in the cerebrospinal fluid indicates subarachnoid bleeding and speaks in favor of a skull fracture. Fracture of the sieve of the nose may be accompanied by nasal liquorrhea, which becomes more noticeable when the head is tilted forward. On the first day after injury, a symptom of nasal liquorrhea is a symptom of a double spot. After the cessation of nasal bleeding, the discharge with nasal liquorrhea acquires a light character and becomes similar to discharge with vasomotor rhinitis. Fractures in the cartilage and bone sections of the nasal septum are accompanied by the formation of a hematoma. The blood poured out after the blow exfoliates the perichondrium and mucous membrane, as a rule, on both sides. Symptoms of hematoma are difficulty in nasal breathing, nasal tone of voice. With anterior rhinoscopy, you can see a cushion-shaped thickening in the initial section of the septum on one or both sides, which has a bright red color. The hematoma tends to suppurate and abscess. In these cases, the headache may increase, the body temperature rises and chills appear. Further development of suppuration of the hematoma of the nasal septum is fraught with melting of the quadrangular cartilage, followed by retraction of the back of the nose and intracranial complications. Treatment Assistance for bruises without bone fractures may be limited to stopping bleeding with cold on the area of injury (in the first hours) and resting the victim. With severe nosebleeds, it is necessary to carry out an anterior loop tamponade, and if it is ineffective, a posterior nasal tamponade should also be performed. The main method of treating fractures of the nasal bones and other skull bones is reposition with subsequent fixation of their fragments. The optimal time for repositioning the nasal bones is considered to be the first 5 hours after injury or 5 days after it. This is due to the development of pronounced swelling of the surrounding soft tissues, which makes it difficult to determine the correct location of the reduced fragments. Reposition is usually performed under local anesthesia (such as lubricating the mucous membrane with a 5-10% solution of cocaine or a 2% solution of dicaine with the addition of 2-3 drops of a 0,1% solution of adrenaline per 1 ml of anesthetic and infiltration anesthesia in the area fracture with a 1-2% solution of novocaine). The reduction of fragments should be done in the supine position of the patient. After the reposition of the nasal bones, their fixation is necessary. In all cases, a loop tamponade of both halves of the nose is performed, which fixes the reduced bones of the external nose and fragments of the deformed nasal septum. When a hematoma of the nasal septum is established, which is confirmed by test puncture with a thick needle, surgical treatment is performed under local anesthesia. Fractures of the maxillary sinus that are not accompanied by visual impairment and significant damage to the walls of the sinus and orbit, confirmed by X-ray examination, are treated conservatively. Puncture of the maxillary sinuses in the first 2 days after injury in order to establish the fact of hemo-sinus and to remove spilled blood is not advisable. However, if on the 3-4th day after the injury signs of inflammation appear (body temperature rises, swelling and pain in the area of the projection of the sinus and lower eyelid), one should think about the transition of hemosinus to pyosinus. In this case, puncture of the maxillary sinus should not be delayed. After removing the pathological contents and washing the sinus with an isotonic solution or furacillin solution, antibiotics are introduced into its cavity. General antibiotic therapy is prescribed. Repeated puncture is performed in accordance with clinical dynamics. Fracture of the paper plate of the ethmoid bone may be accompanied by damage to one of the ethmoid arteries. Bleeding from this artery leads to an increase in pressure in the orbit, exophthalmos and circulatory disorders in the eyeball, which can lead to blindness within a few hours. A timely draining medial paraorbital incision with loose tamponade of the orbital tissue can save vision. To combat liquorrhea and prevent the development of intracranial complications, the patient is prescribed strict bed rest for 3 weeks. The position of the patient in bed is semi-sitting. Restriction of fluid intake and dry eating are prescribed. Regular lumbar punctures are performed to reduce intracranial pressure. Desirable, especially during the first week after injury, prolonged loop tamponade of the nose. General and local antibiotic therapy is prescribed. If within 3-4 weeks the liquorrhea is not eliminated, the question is raised about the surgical plasticity of the cerebrospinal fluid fistula. For fractures of the frontal sinuses, surgical treatment is performed. Depressed bone fragments of the anterior wall, which retain their connection with soft tissues, are carefully repositioned. In the treatment of patients with frontal-basal fractures, the participation of a neurosurgeon and other related specialists is mandatory. Surgical treatment is possible only when the patient's condition is stable. 2. Gunshot wounds of the nose and paranasal sinuses Gunshot wounds of the nose and paranasal sinuses can be divided into three groups: 1) not penetrating into the nasal cavity and paranasal sinuses; 2) penetrating wounds with damage to the bone formations of the nasal cavity and paranasal sinuses; 3) combined injuries with damage to adjacent organs and anatomical structures (cranial cavity, orbits, ears, maxillofacial zone). The most important feature of gunshot wounds is the wound channel with all its properties. Shrapnel wounds cause more severe damage. Also, significant damage is inflicted by a bullet with an unstable center of gravity. Numerous bone walls and formations that form the facial skull also affect the nature of the wound channel. The presence of inlet and outlet holes indicates a through wound, and the size of the inlet is often less than the size of the outlet. In cases where a wounding projectile passing through soft tissues and bone gets stuck in the wound channel, they speak of a blind wound. Isolated blind wounds to the nose and paranasal sinuses are not particularly dangerous. A bullet or fragment, having passed through the soft tissues and bones of the facial skeleton, gets stuck in one of the sinuses, causing their purulent inflammation. Gunshot wounds of the nose and paranasal sinuses are much more dangerous for life, in which adjacent areas are damaged - the cranial cavity, eye sockets, the base of the skull, and the pterygopalatine fossa. The danger of such combined injuries is due to the location of vital organs and structures in these areas. Small foreign bodies in blind gunshot wounds tend to encapsulate. Large foreign bodies, especially those located near vital organs, usually lead to progressive complications. In the diagnosis of foreign bodies of gunshot origin, various x-ray arrangements, linear and computed tomography are used. The nasal cavity, as well as wound channels, can be used for the introduction of radiopaque probes, which help to navigate in the localization of a foreign body. Taking into account the difficulties of removing foreign bodies, as well as the possibility of developing dangerous functional and other (visual, intracranial) complications, V. I. Voyachek proposed a scheme that should be followed to establish indications for an operation to remove them. The scheme is based on four main combinations. All foreign bodies are divided into: 1) easily retrievable; 2) hard-to-recover; 3) causing any disorders (according to the reaction caused by these bodies); 4) do not cause any disorders. There are four combinations: 1) easily accessible, but causing disorders, - removal is mandatory; 2) easily accessible, but not causing disorders - removal is indicated under favorable conditions; 3) hard-to-reach, but not causing disorders - the operation is either contraindicated in general, or is done in case of dangers that threaten the wounded in the further course of the injury; 4) hard-to-reach, but accompanied by disorders of the corresponding functions - extraction is indicated, but due to the complexity of the operation, it must be carried out with special precautions. Lecture No. 11. Diseases of the nose and paranasal sinuses. Foreign bodies in the nose and paranasal sinuses 1. Foreign bodies of the nose and paranasal sinuses Most often, foreign bodies are found in children. In adults, foreign bodies enter the nose under random circumstances. Larger foreign bodies are found only in the mentally ill. Foreign bodies of the nose and paranasal sinuses are possible as a result of gunshot wounds, when wounded with a cold weapon or some household object, the tip of which, fixed in the bone tissues of the nasal cavity, breaks off. Foreign bodies introduced through the nasal vestibule are usually located between the inferior turbinate and the nasal septum. Foreign bodies that enter the nasal cavity in another way can be localized anywhere. A foreign body that is not removed in the near future gradually becomes overgrown with granulations. The carbon dioxide and phosphate salts of calcium that fall out around it form a nasal stone - rhinolith. Rhinoliths can be of the most varied shapes and sizes and sometimes form a cast of the nasal cavity. Clinic A foreign body that has entered the nasal cavity reflexively causes sneezing, lacrimation, and rhinorrhea. Gradually, reflexes fade and the body adapts to a foreign object. The presence of a foreign body in the nose causes the following symptoms: 1) unilateral nasal congestion; 2) unilateral purulent runny nose; 3) unilateral headaches; 4) nosebleeds. Diagnosis The presence of a foreign body helps to establish an anamnesis, rhinoscopy, probing and radiography. The formation of bleeding granulations around a foreign body, narrowing of the nasal passage and purulent discharge can simulate other diseases. In differential diagnosis, age matters: foreign bodies are more common in children, and inflammation of the paranasal sinuses due to their underdevelopment is an exception. Treatment Removal of foreign bodies in recent cases is not particularly difficult. Sometimes they can be removed by blowing the nose (it is better to drip vasoconstrictor drops before that). If this procedure is not successful, then after anemization and anesthesia of the nasal mucosa, the foreign body can be removed using an instrument. The most suitable for this purpose is a blunt hook, which is inserted behind the foreign body and, during the reverse movement, captures and removes it. Attempts to remove a foreign body with tweezers can lead to pushing it deep into the nose. Removal of living foreign bodies is desirable to precede them with immobilization (impact of anesthetics), or in cases with a leech, pour a 10% solution of common salt into the nasal cavity, which will cause its contraction. Removal of very large foreign bodies is possible only through an operation, the volume of which is determined depending on the size and location of the foreign body. 2. Nosebleeds Causes of nosebleeds are divided into local and general. Local causes include: 1) injuries of the nose and paranasal sinuses; 2) atrophic processes of the mucous membrane of the anterior part of the nasal septum, accompanied by the formation of crusts, the removal of which violates the vascular wall; 3) malignant tumors of the nose and paranasal sinuses; 4) benign tumors (angiomas, angiofibromas); 5) foreign bodies of the nasal cavity. Common causes of nosebleeds: 1) arterial hypertension and atherosclerosis; 2) acute infectious lesions of the upper respiratory tract, predominantly of viral origin; 3) septic conditions (chroniosepsis), intoxication, including alcohol; 4) diseases of internal organs (cirrhosis of the liver, chronic glomerulonephritis, heart defects, emphysema, pneumosclerosis); 5) neurovegetative and endocrine vasopathies observed in girls during puberty, in girls and women with impaired ovarian function, with toxicosis of the second half of pregnancy, vicarious (replacing) nosebleeds with delayed menstruation; 6) hypo- and beriberi; 7) decrease in atmospheric pressure, physical overstrain and overheating. Most often, nosebleeds occur in the anteroinferior part of the nasal septum, which is associated with the peculiarity of the blood supply to this area. It is in this place that the terminal branches of the arteries that supply the nasal septum end. The arterial and venous network forms here several layers of the choroid plexus, which is easily injured. The heaviest bleedings are observed from posterior parts of the nasal cavity (basin of the external carotid artery). Bleeding from this area is more often observed in patients with hypertension and atherosclerosis. In nose injuries, bleeding usually occurs from the upper sections, supplied from the anterior ethmoid artery (basin of the internal carotid artery). Clinic and diagnostics If bleeding occurs from the anteroinferior sections of the nasal septum, then it can be easily detected with anterior rhinoscopy. With bleeding from the deep parts of the nasal cavity, the source of hemorrhage in most cases cannot be established. Nosebleeds can occur suddenly. Sometimes it is preceded by prodromal phenomena (headache, tinnitus, dizziness, general weakness). Usually one side bleeds. The intensity of bleeding is different - from small to massive, profuse. The most severe, life-threatening are the so-called signal nosebleeds, which are characterized by suddenness, short duration and an abundance of outflowing blood. After spontaneous cessation of bleeding, severe collapse develops. Signal nosebleeds are a sign of a violation of the integrity of a large arterial vessel in the nasal cavity, the bones of the facial skeleton, the base of the skull in severe trauma, exfoliating aneurysm, a decaying malignant tumor. Such nosebleeds are an indication for urgent hospitalization of the patient in a hospital. In some cases, there is a problem of differential diagnosis between nosebleeds and bleeding from the lower respiratory tract, as well as from the esophagus and stomach. Blood with pulmonary bleeding is foamy, bleeding is accompanied by a cough, with gastric bleeding - dark, clotted. It should be borne in mind that swallowing blood during nosebleeds is accompanied by vomiting with clots of dark, brown coagulated blood mixed with gastric contents, as in gastric bleeding. However, the runoff of scarlet blood along the back wall confirms nosebleeds. Treatment In case of bleeding from the anterior part of the nasal septum, it should be stopped by pressing the bleeding half of the nose against the nasal septum with the fingers of the wing of the nose. In anticipation of the nose, it is better to additionally introduce an adequate lump of cotton - dry or moistened with a 3% hydrogen peroxide solution. The patient should not tilt his head back, as this compresses the jugular veins in the neck, and bleeding may increase. If the listed measures remain unsuccessful, they resort to anterior tamponade, and in case of its insufficiency, to the posterior nasal tamponade. The most famous methods are Mikulich, Voyachek and Likhachev. All types of nasal tamponade in case of epistaxis should preferably be performed after preliminary anesthesia of the mucous membrane with 5-10% cocaine solution or 2% dicaine solution. However, during ongoing bleeding, this is not always possible. Tamponade, depending on the condition of the patient, is performed in a sitting or lying position. Anterior nasal tamponade according to Mikulich. It is carried out most quickly and simply. The corresponding nostril is expanded by the nasal planum. A tampon prepared from a gauze bandage 1-2 cm wide and up to 70 cm long, impregnated with vaseline oil, is inserted into the nasal cavity with the help of a forceps to a depth of 6-7 cm. It is necessary to ensure that the instrument that introduces the tampon is directed to the choana along the bottom of the nose, and not to its arch. The patient's head should not tilt back. Gradually, the entire tampon fits into the nasal cavity according to the "accordion" principle from the bottom up until it densely fills the corresponding half of the nose. The excess of the tampon is cut off, and the remaining end is wound on cotton wool. Posterior nasal tamponade. This type of stopping nosebleeds is resorted to when all other methods have been exhausted. The rear cotton-gauze swab for the nasopharynx is prepared and sterilized in advance. The optimal size of the tampon should correspond to the terminal phalanges of the thumbs, folded together. The tampon is tied crosswise with two thick strong threads. After local anesthesia, a rubber catheter is inserted through the bleeding half of the nose into the oropharynx, the end of which is brought out through the mouth with the help of a forceps. Both threads are tied to the withdrawn end of the catheter. When the catheter is brought back through the nose, thanks to the threads tied to it, the tampon is inserted into the nasopharynx, tightly pulling up to the choanae. Keeping the threads in a taut state, anterior nasal tamponade is performed. The tamponade ends by tying threads over a cotton or gauze "anchor" with a bow, which allows, if necessary, to tighten the displaced nasopharyngeal tampon. The third thread of the tampon is placed without tension between the cheek and the gum of the lower jaw and its end is fixed with a strip of adhesive plaster on the cheek or in the ear area on the side of the tamponade. For this thread, the tampon is removed from the nasopharynx after preliminary untying or cutting the bow and removing the front tampons. It is desirable to impregnate the nasopharyngeal swab with antibiotics, as well as hemostatic preparations. It should be, like other tampons, lubricated with vaseline oil. To avoid infection, swabs are kept in the nasal cavity for 2 days. A longer stay of tampons in the nasal cavity and in the nasopharynx is fraught with the development of sinusitis and otitis media. All types of nasal tamponade are completed by the imposition of a horizontal or, if the back of the nose is injured, a vertical sling-like bandage. Surgical ways to stop nosebleeds. They are used for the ineffectiveness of tamponade and recurrent nosebleeds. In order to obliterate the vessels of the mucous membrane of the nasal septum, various sclerosing preparations are used (0,5-1 ml of a 5% solution of quinine dihydrochloride). Most often, with repeated nosebleeds from the anterior part of the nasal septum, the mucous membrane is detached in the area of bleeding, followed by tamponade. If the source of epistaxis is the ethmoid arteries (branches of the internal carotid artery), endonasal opening of the ethmoid labyrinth on the bleeding side is possible. The resulting cavity after the opening of the lattice cells is tightly plugged. In case of persistent bleeding coming from the pool of the external carotid artery, clipping of the maxillary artery through the maxillary sinus is possible. Among the methods of stopping nasal bleeding by ligation of the main vessel throughout, the most common is the ligation of the external carotid artery (provided that bleeding comes from a vessel belonging to its pool). Ligation of the external carotid artery is a serious surgical intervention that requires sufficient surgical preparedness of the doctor and knowledge of the topographic anatomy of the neck. One common approach to the external carotid artery is along the anterior edge of the sternocleidomastoid muscle. It should be borne in mind that in patients suffering from certain general diseases, epistaxis develops as a result of a violation of homeostasis. In this regard, along with local measures to stop bleeding and compensate for blood loss, efforts must be made to eliminate the causes that caused nosebleeds. Lecture number 12. Diseases of the nasal cavity 1. Deviated septum Deviated septum is one of the most common rhinological pathologies. The causes of frequent deformation can be anomalies in the development of the facial skeleton, as well as rickets, injuries. Due to the fact that the nasal septum consists of various cartilaginous and bone structures, limited above and below by other elements of the facial skull, the ideal and combined development of all these components is extremely rare. Variations of the curvature of the nasal septum are very different. Possible shifts in one direction or another, s-shaped curvature, the formation of ridges and spikes, subluxation of the anterior quadrangular cartilage. Most often, the deformation is observed at the junction of individual bones and quadrangular cartilage. Particularly noticeable curvatures are formed at the junction of the quadrangular cartilage with the vomer and the perpendicular plate of the ethmoid bone. Deformation of the nasal septum, causing a violation of the function of external respiration, determines a number of physiological abnormalities that were mentioned when considering the function of the nose. In the nasal cavity itself, respiratory defects reduce the gas exchange of the paranasal sinuses, contributing to the development of sinusitis, and the difficulty in the flow of air into the olfactory gap causes a violation of smell. Clinic The leading symptom of a clinically significant curvature of the nasal septum is unilateral or bilateral obstruction of nasal breathing. Other symptoms may be a violation of the sense of smell, nasal, frequent and persistent rhinitis. Diagnostics It is established on the basis of a cumulative assessment of the state of nasal breathing and the results of rhinoscopy. It should be added that the curvature of the nasal septum is often combined with deformity of the external nose of congenital or acquired (usually traumatic) origin. Treatment Treatment is surgical only. The indication for surgery is difficulty in nasal breathing through one or both halves of the nose. Operations on the nasal septum are also performed as a preliminary stage preceding other surgical interventions or conservative methods of treatment. Operations on the nasal septum are performed under local or general anesthesia. Damage to the mucosa in adjacent areas of the septum leads to the formation of persistent, practically unrepairable perforations. Bloody crusts dry up along the edges of the latter. Large perforations contribute to the development of atrophic processes, small ones cause whistling during breathing. Various modifications of operations on the nasal septum are used, we will consider a few. The first is a radical submucosal resection of the nasal septum according to Killian, the second is a conservative septum operation according to Voyachek. In the first method, most of the cartilaginous and bony skeleton of the septum is removed. The advantage of this operation is its comparative simplicity and speed of execution. Disadvantages - observed during breathing flotation of the nasal septum, devoid of most of the bone and cartilage framework, as well as a tendency to develop atrophic processes. In the second method, only those parts of the cartilaginous and bone skeleton are removed that cannot be redressed and placed in the correct median position. With a curvature of the quadrangular cartilage, the disk is cut out by circular resection. As a result, the disk, which retains contact with the mucous membrane of one of the parties and has acquired mobility, is set to the middle position. Conservative methods of surgery on the nasal septum are more surgically complex interventions. However, their long duration and possible moderate reactive phenomena in the nasal cavity in the first weeks after the operation pay off in the future by maintaining an almost complete nasal septum. 2. Bleeding polyp of the nasal septum This disease is often encountered in clinical practice. Its characteristic feature is the appearance in the anterior part of the nasal septum on one side of a gradually increasing polyposis formation, which bleeds easily. Etiology The etiology is not always clear. One of the reasons for the appearance of a polyp is trauma to the mucous membrane with fingernails in the area of its increased vascularization. The disease is more common in young people and in women during pregnancy and lactation, which indicates the possible importance of endocrine factors in its formation. In morphological examination, as a rule, hemangioma is observed, in more rare cases - granulation tissue. Clinic The main complaint of the patient: difficulty in nasal breathing and frequent, profuse nosebleeds, recurring when blowing the nose, touching with a finger. Rhinoscopy allows you to detect a polyposis formation of red or purple-red color. The stalk of the polyp is usually wide. When probing, the polyp bleeds easily. Diagnosis is based on history and anterior rhinoscopy. Treatment Only surgical. The polyp should be removed along with the adjacent mucosa and perichondrium of the nasal septum. After removal, it is desirable to perform electrocaustics or cryoapplication of the mucous membrane along the edge of the wound surface, followed by tamponade. 3. Anterior dry rhinitis. Perforating ulcer of the nasal septum Anterior dry rhinitis occurs in the anterior part of the nasal septum at the site of frequent trauma to the mucous membrane. Clinic Patients complain of a feeling of dryness in the nose, drying of the crusts in the vestibule of the nose, which causes the need for their removal. With rhinoscopy in the anterior part of the nasal septum, a limited area of dry, thinned mucous membrane is determined, which has lost its normal wet sheen, covered with dry crusts. Then a through defect of the nasal septum may occur at this place. Perforation is usually small, rounded. It often closes with dry crusts, the removal of which may lead to bleeding, as well as wheezing, noticeable with forced breathing. Diagnosis Diagnosis is based on history and anterior rhinoscopy. Differential diagnosis The differential diagnosis is carried out with tuberculosis, syphilis and Wegener's disease. Treatment Based on the same principles as the treatment of atrophic rhinitis. 4. Inflammatory diseases of the nasal cavity. Acute rhinitis. Acute catarrhal (nonspecific) rhinitis Acute rhinitis is an acute disorder of the nasal function, accompanied by inflammatory changes in the mucous membrane. Acute rhinitis can be an independent inflammation of the nasal cavity, as well as accompany many infectious diseases. In the definition of acute nonspecific rhinitis, the term "catarrh" is widely used, which characterizes not so much a superficial process as a pathological condition, accompanied by an increased separation of fluid from the surface of the mucous membrane. Etiology and pathogenesis In the etiology of acute rhinitis, low-virulence saprophytic flora, various factors of a non-infectious nature, such as mechanical and chemical irritants, matter. In acute traumatic rhinitis, activation of the permanent microflora of the nasal cavity is noted, the action of which is added to the irritation caused by trauma. In the pathogenesis of acute infectious rhinitis, the cooling factor plays a leading role. Cooling contributes to the activation of the saprophytic flora and the acquisition of pathogenicity by it, leads to a slowdown or complete cessation of the movement of the cilia of the ciliated epithelium. As a result, the pathogenic factor does not move with cilia to the nasopharynx, where, due to pharyngeal reflexes, it spits out along with mucus or, when it enters the stomach, is exposed to gastric juice, but penetrates deep into the epithelium, causing an inflammatory reaction. Clinic Symptoms of acute rhinitis include congestion of the mucous membrane, swelling of the turbinates, feeling hot, sneezing, and watery eyes. If the turbinates are significantly enlarged, then patients may experience an unpleasant feeling of complete blockage of the nose. Nasal congestion is often accompanied by a feeling of heaviness in the head, dull pain in the forehead. Functional disorders are manifested by a violation of nasal breathing, smell, a change in the timbre of the voice and secretion. Difficulty in breathing caused by obstruction of the nasal lumen leads to the exclusion of protective reflexes emanating from the receptor field of the nasal cavity. The patient is forced to breathe through the mouth, which contributes to the development of inflammation of the mucous membrane of the underlying respiratory tract. In the first period of a runny nose, the nasal mucosa is drier than normal (hyposecretion). Then it is replaced by hypersecretion, first in the form of a transudate, and then with a thicker mucopurulent discharge. In the clinic of acute rhinitis, there are three stages. The first stage (dry stage) is characterized by a feeling of dryness, burning, feeling of tension in the nose. The mucous membrane is hyperemic, has a dry sheen. There is sneezing, coughing. The volume of the turbinates increases significantly, as a result of which only the inferior turbinates are visible during anterior rhinoscopy. Nasal breathing can be completely switched off, resulting in anosmia and decreased taste sensations. A nasal tone of speech appears. The onset of the disease may be preceded by a feeling of malaise, weakness, slight chilling, a slight increase in body temperature. The duration of the first stage is from several hours to 1-2 days. The second stage (the stage of serous discharge) begins with a copious discharge of a completely transparent watery fluid (transudate). During this period, the sensations of burning and dryness decrease. The mucous membrane acquires a cyanotic hue, its moisture content increases, and an increased amount of discharge is observed in the lower and common nasal passages. The edema of the turbinates decreases, nasal breathing improves. The third stage (the stage of mucopurulent discharge) occurs on the 3rd - 5th day of rhinitis, is characterized by a gradual decrease in the amount of discharge, which becomes more and more thick. Inflammatory changes in the nose gradually decrease. Acute rhinitis can last from 1 to 2-3 weeks or more. An abortive course lasting 2-3 days is also possible. Treatment When the first signs of malaise appear, general warming (hot baths), ingestion of 2-3 glasses of hot tea, wrapping and bedding are recommended. At the same time, oral administration of acetylsalicylic acid (0,5-1,0 g) is indicated to stimulate the "pituitary - adrenal cortex" system. Various effects on reflexogenic zones are also widely used (dry mustard in stockings, hot foot baths, erythemal dose of ultraviolet radiation on the nose and face, feet, calf muscles, lower back). However, all these measures give the expected result only at the very beginning of the disease. Drug treatment of catarrhal rhinitis mainly consists in the use of vasoconstrictor drugs in the nose and the appointment of antihistamines (diphenhydramine, tavegil, suprastin, diazolin). Taking vasoconstrictor drugs is most rational in the first stage of the common cold, when there is a pronounced swelling of the mucous membrane, which disrupts nasal breathing and gas exchange in the paranasal sinuses. Taking these drugs for more than 8-10 days affects the vasomotor function of the mucous membrane. There is a danger of developing vasomotor rhinitis, the restoration of the function of the ciliated epithelium is disturbed. In the future, an allergic reaction to any drug injected into the nose is possible, as well as the development of hypertrophic and atrophic rhinitis. A 0,5-0,1% solution of naphthyzine, a 0,05-0,1% solution of galazolin, a 0,1% emulsion of sanorin, as well as a 2-3% solution of ephedrine have a good vasoconstrictor effect. With a pronounced inflammatory reaction in the nasal cavity, various antimicrobial drugs can be prescribed (2-5% solution of collargol or protargol, 20% solution of sulfacyl, injection of sulfonamide and antibiotic powders into the nose). However, elevated concentrations of antibiotics and sulfonamides inhibit the function of the ciliated epithelium, which slows down the healing process. Lecture No. 13. Diseases of the nasal cavity. Chronic rhinitis. atrophic rhinitis. Vasomotor rhinitis 1. Chronic catarrhal rhinitis Chronic catarrhal rhinitis develops as a result of recurrent acute rhinitis. Prolonged congestive hyperemia of the nasal mucosa caused by alcoholism, a chronic disease of the cardiovascular system, kidneys predisposes to the development of chronic rhinitis. In the etiology of the disease, hereditary prerequisites, malformations, violations of normal anatomical relationships that cause difficulty in nasal breathing may be important. Chronic runny nose also develops as a secondary disease in the pathology of the nasopharynx and paranasal sinuses. Clinic The symptoms of chronic catarrhal rhinitis basically correspond to those of acute rhinitis, but are much less intense. The patient complains of discharge from the nose of a mucous or mucopurulent nature. Difficulty in nasal breathing is aggravated (as is discharge from the nose) in the cold. Often there is an alternating congestion of one of the halves of the nose. With rhinoscopy, diffuse hyperemia of the mucous membrane is determined, often with a cyanotic tint. The inferior turbinates are moderately swollen, narrowing the lumen of the common nasal passage. Chronic catarrhal rhinitis may be accompanied by hyposmia. The transition of catarrhal inflammation from the nasal cavity to the mucous membrane of the auditory tube is possible, followed by the development of tubo-otitis. Diagnosis The diagnosis of the disease is established on the basis of complaints, anamnesis, anterior and posterior rhinoscopy. Differential diagnostics To distinguish catarrhal chronic rhinitis from hypertrophic, anemization of the mucous membrane is performed with vasoconstrictor agents. A noticeable reduction in the mucous membrane of the turbinates indicates the absence of true hypertrophy, characteristic of hypertrophic rhinitis. Differential diagnosis between false and true hypertrophy can also be made using a bellied probe. In the case of false hypertrophy, the probe bends the mucous membrane to the bone wall more easily. With true hypertrophy, a compacted tissue is determined, which is hardly amenable to the pressure exerted on it. Treatment It is necessary to eliminate the adverse factors that cause the development of chronic rhinitis. It is useful to stay in a dry warm climate, hydro- and balneotherapy is indicated. Local treatment consists in the use of antibacterial and astringent preparations in the form of a 3-5% solution of protargol (collargol), 0,25 - 0,5% solution of zinc sulfate, 2% salicylic ointment, etc. UHF is prescribed for the area nose, endonasal UVI (quartz tube). The prognosis is usually favorable. 2. Chronic hypertrophic rhinitis The causes of hypertrophic rhinitis are the same as catarrhal. Clinic Hypertrophic rhinitis is characterized by persistent nasal congestion. Complicates nasal breathing and abundant mucous and mucopurulent discharge. Obstruction of the olfactory fissure leads to hyposmia and further anosmia. In the future, as a result of atrophy of the olfactory cells, essential (irreversible) anosmia may occur. The timbre of the voice in patients becomes nasal. As a result of compression of the lymphatic slits by the fibrous tissue, the lymphatic drainage from the cranial cavity is disturbed, which causes a feeling of heaviness in the head, disability and sleep disturbance. Treatment Treatment of hypertrophic rhinitis is predominantly surgical. If there is bone hypertrophy of the turbinates, one of the options for submucosal intervention is performed. With limited hypertrophy of the anterior and posterior ends of the inferior turbinates or their lower edge, these sections are excised (conchotomy). These surgical interventions are usually performed under local anesthesia (such as lubrication of the mucous membrane with 3-10% cocaine solution or 2% dicaine solution with the addition of 2-3 drops of 0,1% adrenaline solution per 1 ml of anesthetic and intracarcinal administration 5 ml of 1-2% solution of novocaine or 0,5% solution of trimecaine). The operation ends with a loop tamponade. The tampons are removed after 2 days. However, given the possibility of significant bleeding after the removal of tampons, especially after cutting off the posterior ends of the inferior turbinates (posterior conchotomy), complete removal of tampons can be performed at a later date. Irrigation of tampons with antibiotic solutions is recommended to prevent infection. 3. Atrophic rhinitis Simple atrophic rhinitis. This form of chronic rhinitis can be primary or secondary. Secondary atrophic rhinitis is a consequence of exposure to various adverse environmental factors. In the development of atrophic rhinitis, various injuries play a role, causing tissue damage and blood supply to the nasal cavity. The process of atrophy can be local and diffuse. Subjective sensations of dryness can be very painful. With anterior rhinoscopy, the posterior wall of the nasopharynx is freely visible. The mucous membrane acquires a dry lacquer sheen and is covered with crusts of dried mucus. When the process captures the olfactory zone, hypo- and anosmia develops. In some cases, patients note an unpleasant odor that is not captured by others. Treatment It is necessary to eliminate or reduce the impact of harmful environmental factors. A course of treatment with ointments and iodine-glycerin is prescribed locally. In the morning and evening, the patient should inject Voyachek's diachilic ointment into the nose on a cotton swab for 10 minutes. 2 times a week, the doctor or the patient himself lubricates the nasal mucosa with a solution of iodine-glycerin. Such treatment is carried out for 2 months and is repeated 3 times a year. It is also recommended to insert cotton swabs into the nose with rosehip or sea buckthorn oil in olive or peach oil in a ratio of 1:3-1:4 or with the addition of an oil solution of vitamin A (no more than 50 IU). Oral intake of vitamin A and a complex of multivitamins with microelements (for example, Vitrum) is also appropriate. Ozen. Ozena is characterized by chronic atrophic fetid rhinitis, characterized by deep atrophy of the entire mucous membrane, as well as the bony walls of the nasal cavity and nasal concha. Ozena is characterized by the release of a thick secret, which dries into fetid crusts. The etiology and pathogenesis of the disease continue to be insufficiently elucidated to date. The infectious nature of ozena is confirmed by the patterns of vegetation of Klebsiella in the human body. This is its constant presence in patients with ozena and its absence in healthy people, as well as in patients with other diseases. In the pathogenesis of ozena, an essential role is played by hereditary-constitutional features that are inherited as a recessive trait, environmental conditions, as well as alimentary and vegetative insufficiency. Clinic Ozena most often develops in people with chameprosopia, i.e., in people with broad faces. The bridge of their nose is usually wide and seems as if pressed down and flattened, and the nasal openings appear to be facing anteriorly and upward. This shape of the nose often resembles the appearance that is observed in some forms of congenital syphilis. The disease usually begins at a young age, women are more often ill. After the onset of menopause, many clinical manifestations of ozena decrease. For patients with ozena, the presence of severe atrophy of the mucous membrane of the nasal cavity, a decrease in the size of the nasal conchas, especially the lower ones, are characteristic. As a result of atrophy of the mucous membrane and turbinates, the nasal cavity becomes wide. With anterior rhinoscopy, not only the posterior wall of the nasopharynx, but also the pharyngeal mouths of the auditory tubes are freely visible. Sometimes the openings of the sphenoid sinus located in the direction of the posterior and upward are visible. Often, during lakes, the entire nasal cavity is filled with crusts to such an extent that neither the mucous membrane nor even the shells themselves can be seen behind them. An extremely unpleasant, fetid odor emanates from the crusts. Actually, of all the objective signs of ozena, the stench should be put in the first place as a constant and most significant objective symptom. Treatment Crusts from the nose are removed by washing the nasal cavity with 2% sodium bicarbonate solution, 1% hydrogen peroxide solution, 0,1% potassium permanganate solution, or saline. For washing, use an Esmarch mug or a special nasal watering can. In order to prevent the washing liquid from getting into the auditory tube and the tympanic cavity, the patient should slightly tilt his head forward and to the side opposite to the washed half of the nose. The mouth opens slightly, and then the washing liquid, pouring in through one half of the nose, pours out through the other. Crusts can also be removed with Gottstein tamponade. Tamponade of both halves of the nose is performed with several gauze turundas or cotton swabs introduced into the nasal cavity with a special narrow spatula. It is better to administer tampons with some ointment (diachylic, alkaline) or with iodine-glycerin for 2-3 hours. When the tampons are removed, fetid crusts go away, and mechanical and medicinal irritation of the nasal mucosa causes an abundant release of liquid mucus. After removing the crusts, the nasal cavity is lubricated with diakhil ointment or iodine-glycerin. In the treatment, antibiotics are used that are active against Klebsiella ozena: streptomycin, monomycin, neomycin, kanamycin, chloramphenicol. In most cases, due to the ineffectiveness of the conservative, they resort to the surgical method of treating ozena. 4. Vasomotor rhinitis (neurovegetative and allergic forms) In the occurrence of the neurovegetative form of vasomotor rhinitis, the main role is given to functional changes in the central and autonomic nervous system, as well as the endocrine system. The development of vasomotor rhinitis is also facilitated by reflex effects, in particular cooling, a sedentary lifestyle, and medications. The allergic form of vasomotor rhinitis occurs when exposed to various allergens, depending on which seasonal and permanent (year-round) forms are distinguished. Pathogenesis The pathogenesis of allergic rhinitis consists in a specific reaction between the allergen and tissue antibodies, as a result of which mediators of the allergic reaction are released, contributing to the development of the clinical manifestations of the disease. Clinic Clinic of the neurovegetative form of vasomotor rhinitis: difficulty in nasal breathing, profuse serous or mucous discharge, bouts of paroxysmal sneezing, sensation of itching and burning in the nasal cavity. The mucous membrane has a cyanotic color. During rhinoscopy, the turbinates appear swollen, when pressed on them with a bellied probe, the latter easily bends the soft tissues to the bone wall without any resistance. Lubrication of the mucous membrane with vasoconstrictor drugs leads to a rapid contraction of the shells. Outside of an attack, the rhinological picture may have a normal appearance. Clinic of seasonal allergic rhinitis (hay fever). Characterized by a clear seasonality of the onset of exacerbation. During this period, there are paroxysms of sneezing, itching and burning in the nasal cavity, eyes, conjunctival hyperemia. Almost complete nasal congestion and severe rhinorrhea occur, which leads to maceration of the skin in the vestibule of the nose. The mucous membrane in the initial period is sharply hyperemic, there is a significant amount of clear liquid in the nose. In the future, the mucous membrane acquires a cyanotic appearance, and then turns pale. In patients during this period, itching in the eyes, hyperemia of the conjunctiva, a feeling of rawness in the throat, larynx and skin itching are often noted. In some cases, the development of angioedema and larynx is possible. There are various uncomfortable manifestations, headache, fatigue, sleep disturbance, fever. The duration of the disease usually corresponds to the period of flowering of plants and stops on its own after it ends or after the patient changes the allergenic area. Clinic of permanent (year-round) form of allergic rhinitis. The disease is chronic. The expressed puffiness of nasal conchas is defined. The mucous membrane is pale. With posterior rhinoscopy, a cushion-like thickening of the vomer mucosa is often noted, expressed on both sides. The middle turbinates are also edematous. When examining the turbinates with a bellied probe, their test density is determined, which does not allow one to feel the bony stroma of the shell. Anemization of the mucous membrane often does not lead to a noticeable reduction in the turbinates. Mucus microscopy reveals a significant number of eosinophilic leukocytes. The allergic form of vasomotor rhinitis is characterized by the formation of mucous polyps, which can fill the entire nasal cavity, in some cases pushing the bone walls apart and deforming the external nose. Often there is a combination of allergic rhinitis with bronchopulmonary pathology - asthmatic bronchitis and bronchial asthma. Treatment Treatment for the neurovegetative form of vasomotor rhinitis is to eliminate the various causes that cause this disease. Various types of intracarcinal disintegration are also used. An active mobile lifestyle is recommended, hardening procedures - short-term dousing of cold water on the soles of the feet. The systematic use of vasoconstrictors is not recommended. Acupuncture, the impact on the reflex zones of the nasal cavity are also used. Treatment of allergic rhinitis includes three main areas, such as elimination therapy, immunotherapy and drug therapy. The goal of elimination therapy is to eliminate allergens. Of the drug therapy, diphenhydramine, diazolin, suprastin, fenkarol, tavegil, pipolfen are most often used. Quite widely used are two aerosol local antihistamines - histimet (levokabastin) and allergodil (acelastin). Topical corticosteroid preparations are used in the form of dry or wet sprays: baconase (beclomethasone dipropionate), syntaris (flunisolide), flixonase (fluticosone propionate). Lecture number 14. Inflammatory diseases of the paranasal sinuses More often, large sinuses are subject to the inflammatory process. 1. Acute sinusitis EtiologyThe etiology of both acute and chronic sinusitis is infectious. The most common way is through natural fistulas that communicate the sinus with the nasal cavity. In acute infectious diseases, infection of the sinuses is possible by the hematogenous route. In the etiology of maxillary sinusitis, purulent foci of the dentition also play a role, especially large and small molars adjacent to the lower wall of the sinus. The most common cause of odontogenic maxillary sinusitis is foreign bodies penetrating into the sinus from the oral cavity: filling material, fragments of broken dental instruments, failed tooth roots, turundas. Granulomas at the root of the tooth, subperiosteal abscesses, periodontal disease can also lead to odontogenic maxillary sinusitis. The most common cause of acute sinusitis is acute respiratory infections. In recent years, a fungal infection of the paranasal sinuses has become relevant. Pathogenesis In the pathogenesis of acute and especially chronic sinusitis, the ventilation of the paranasal sinuses is important, caused by anatomical defects in the nasal cavity (such as a pronounced curvature of the nasal septum, hypertrophy of the middle turbinates), as well as congenital narrowness of the nose (leptorinia). When the sinus fistula is closed with an edematous mucosa, the oxygen content in the sinus will decrease, and the carbon dioxide content will increase. The oxygen content drops especially if pus is produced in the sinus. In the presence of pus, the oxygen content in the sinus approaches zero, while the carbon dioxide content increases significantly, and the pH value decreases. Oxygen is absorbed not only by the mucous membrane, but also by bacteria and leukocytes. All this contributes to the development of anaerobic infection in chronic sinusitis. Allergic processes and immunological deficiency play a significant role in the development of acute and chronic sinusitis. Of no small importance in the development of acute and chronic sinusitis is a violation of the normal function of the mucociliary apparatus of the mucous membrane, caused by adverse environmental factors, such as cold air, atmospheric pollution with harmful gases of industrial production. As a result, inhibition or cessation of the beating of the cilia occurs, which leads to a delay in the infectious onset in the nasal cavity and paranasal sinuses and its subsequent penetration through the membranes of the mucous membrane. Chronic diseases, including diabetes mellitus, contribute to the development of acute and especially chronic sinusitis. Clinic The characteristic symptoms for all sinusitis are congestion of the corresponding half of the nose (with a bilateral process - both halves), mucous or purulent discharge from the nose, the presence of a purulent path in the middle or upper nasal passage, and a violation of the sense of smell. Local symptoms in sinusitis are due to the localization of the process. Diagnosis of sinusitis is based on the assessment of complaints, anamnesis of the disease, identification of general and local symptoms, radiation diagnostics and methods of instrumental examination (puncture, trepanopuncture and probing of the paranasal sinuses). Acute ethmoiditis. The lattice labyrinth is the first to be exposed to any adverse environmental factors. The narrow excretory ducts of individual parts of the labyrinth easily overlap with swelling of the mucous membrane, which contributes to the development of the inflammatory process in the cellular structures of the ethmoid bone. Typical symptoms: fever and headaches. Locally, the disease manifests itself in a feeling of soreness, localized in the region of the root of the nose and at the inner corner of the eye, aggravated by palpation. Patients note nasal congestion, abundant mucopurulent and purulent discharge, impaired sense of smell. The latter can manifest itself as hypo- and anosmia and is due to swelling of the olfactory zone (respiratory anosmia). With damage to the olfactory nerve, anosmia is essential in nature. During anterior rhinoscopy, hyperemia and edema of the mucous membrane in the region of the middle nasal passage and middle nasal concha, accumulation of pus in the middle nasal passage are determined. With posterior rhinoscopy, purulent discharge can also be detected in the upper nasal passage, since in acute inflammation all groups of cells of the ethmoid labyrinth are affected. In cases where, as a result of mucosal edema, a purulent path is not detected, it is recommended to anemize it and repeat rhinoscopy after a few minutes. If there is a violation of the discharge of pus (with a closed empyema), eye symptoms may appear. Acute maxillary sinusitis (sinusitis). At the same time, sinusitis patients are worried about headache, localized in the area of the projection of the maxillary sinus. However, in many cases, its distribution was noted in the forehead, zygomatic bone, and temple. It can radiate to the orbital region, to the upper teeth. Very characteristic is the intensification and sensation of a rush of heaviness in the corresponding half of the face when the head is tilted forward. Headache is associated with secondary trigeminal neuralgia and a violation of the barofunction of the sinus as a result of mucosal edema and blockage of the anastomosis. There may be swelling of the cheek on the affected side. Palpation in the projection of the sinus increases pain. Severe swelling of the face, as well as the eyelids, is more characteristic of complicated sinusitis. Patients note nasal congestion and mucous or purulent discharge, as well as a decrease in the sense of smell on the side of inflammation. Anterior rhinoscopy allows you to establish hyperemia and swelling of the mucous membrane of the lower and especially the middle turbinate. The presence of serous or purulent discharge in the middle nasal passage is characteristic, which can also be established with posterior rhinoscopy. In cases where no discharge is detected (with severe swelling of the mucous membrane that overlaps the anastomosis), it is also recommended to anemize the area of the middle nasal passage and turn the patient's head in a healthy direction. In this position, the sinus outlet is at the bottom, and pus (if any) will appear in the middle nasal passage. As a result of turbinate edema, as with ethmoiditis, respiratory hemi- and anosmia is possible. In the case of toxic damage to the olfactory nerve, anosmia may be essential. In clinical practice, there is a frequent combination of acute maxillary sinusitis and ethmoiditis. Acute frontal. This disease, along with the general symptoms characteristic of a febrile state, is characterized by a strong, sometimes acute headache, localized mainly in the forehead, and a feeling of heaviness in the projection of the affected sinus. Percutere there is also an increase in pain, and when stroking the skin, a feeling of velvety may appear, which in this case indicates the phenomenon of periostitis. With finger pressure in the region of the medial angle of the eye and on the orbital (thinnest) wall of the frontal sinus, pain almost always increases with acute frontal sinusitis. Often there is swelling of the upper eyelid, expressed to one degree or another. Purulent discharge is localized in the most anterior sections of the middle nasal passage, according to the location of the excretory duct. Acute sphenoiditis is an inflammation of the sphenoid sinus. It is also often associated with inflammation of the ethmoid labyrinth, with posterior cells usually involved (posterior ethmoiditis). In acute sphenoiditis, patients complain of severe, "split head" headaches, often radiating to the back of the head and orbit. A characteristic feature is the flow of purulent mucus along the back of the pharynx, which is established during mesopharyngoscopy. Anterior deep rhinoscopy allows you to see a symptom of imaginary infection - the closure of the hyperemic mucous membrane of the posterior parts of the middle nasal concha and the nasal septum, which indicates the involvement of cells of the ethmoid labyrinth (usually posterior) in the process. After anemia and contraction of the mucous membrane in the region of the olfactory fissure, a strip of pus is likely to appear. Posterior rhinoscopy reveals accumulation of pus in the nasopharyngeal vault, the mucous membrane of the nasopharynx and the posterior edge of the vomer is hyperemic and edematous. Disturbance of smell is characteristic. Diagnosis The diagnosis of acute sinusitis is established on the basis of complaints, anamnesis, described symptoms and the results of an X-ray examination. On radiographic images, acute sinusitis is characterized by homogeneous darkening of the sinuses involved in the inflammatory process. If the picture is taken in the vertical position of the subject, then if there is exudate in the sinus, the fluid level can be observed. Diagnostic and at the same time therapeutic methods include punctures and probing of the paranasal sinuses. Treatment Treatment of uncomplicated acute sinusitis is usually conservative. It can be done on an outpatient basis and in an inpatient setting. Polysinusitis, as well as sinusitis, accompanied by severe headache, swelling of the soft tissues of the face and the threat of developing ophthalmic and intracranial complications, should be treated in a hospital. Treatment of acute sinusitis, like other focal infections, consists of a combination of general and local methods. The local treatment is based on the anemization of the nasal mucosa, which can be carried out using official vasoconstrictors (naphthyzinum, sanorin, galazolin). More effective is targeted smearing by the doctor of the mucous membrane in the area of the middle nasal passage with a 3-5% solution of cocaine or an anesthetic - a 2% solution of dicaine with 3-4 drops of a 0,1% solution of adrenaline per 1 ml of the drug. Anemization of the mucous membrane and a decrease in its volume contribute to the expansion of the fistulas of the sinuses and facilitate the outflow of exudate. This is also facilitated by thermal procedures (sollux, diathermy, UHF). Correctly applied to the corresponding half of the face, the compress improves microcirculation in the area of the inflammatory process, reduces swelling of the soft tissues of the face and the mucous membrane of the nasal cavity, restoring the patency of the anastomoses and drainage of the sinuses. UHF is poorly tolerated by patients with vascular disorders, including those with vegetative-vascular dystonia. The puncture of the maxillary sinuses remains one of the most common methods of conservative treatment. Other methods of conservative treatment - trepanopuncture of the frontal sinuses, puncture of the ethmoid labyrinth, puncture and probing of the sphenoid sinus - are more complex manipulations and are carried out in stationary conditions. If repeated punctures of the paranasal sinuses are necessary, permanent drainages are used, which are thin polyethylene or fluoroplastic tubes that are inserted into the sinus for the entire period of treatment, saving the patient from unpleasant manipulations. Through the introduced drainage tube, the sinuses are systematically washed with an isotonic or furatsilin (1: 5000) solution and other drugs (usually antibiotics) are administered. The introduction of medicinal solutions into the paranasal sinuses is possible by the method of movement. With this method, a vacuum is created in the nasal cavity with the help of surgical suction. It allows you to remove pathological contents from the sinuses, and after infusion of medicinal solutions into the nasal cavity, the latter rush into the opened sinuses. As a general treatment for patients with acute sinusitis, analgesics, antipyretics, antihistamines and antibacterial drugs are prescribed. Penicillin can be prescribed at 500 IU 000-4 times a day, as well as other antibiotics with a wider spectrum of action (tseporin, keflin, kefzol). The prescription of antibiotics should be adjusted in accordance with the sensitivity of the microflora obtained from the focus of inflammation. Sulfa drugs (sulfadimethoxine, sulfalene, biseptol) are prescribed both independently and in combination with antibiotics. In case of odontogenic maxillary sinusitis, the corresponding carious teeth should be removed. In this case, an undesirable opening of the maxillary sinus is possible. The resulting channel connecting the sinus with the oral cavity (oroantral fistula) can close on its own or after repeated lubrication with iodine tincture. Otherwise, they resort to plastic closure of the fistula by moving a flap cut from the soft tissues of the gums. 2. Chronic sinusitis Chronic sinusitis usually results from repeated and insufficiently treated acute sinusitis. A combination of adverse factors of a general and local nature, such as a decrease in the body's reactivity, impaired drainage and aeration of the sinus, caused by anatomical abnormalities and pathological processes in the nasal cavity, as well as dental diseases, is essential in their development. The variety of pathomorphological changes in chronic sinusitis, representing various variants of exudative, proliferative and alterative processes, determines the diversity of clinical and morphological forms and the difficulties of their classification. Currently, the classification of chronic sinusitis proposed by B. S. Preobrazhensky (1956) continues to be the most acceptable. According to this classification, there are exudative (catarrhal, serous, purulent) and productive (parietal-hyperplastic, polypous) forms of sinusitis, as well as cholesteatoma, necrotic (alternative), atrophic and allergic sinusitis. With exudative forms, a pattern of diffuse inflammatory infiltration by lymphocytes, neutrophils and plasma cells is observed. It is more pronounced with purulent than with catarrhal and serous forms. In these cases, the epithelium is flattened, metaplastic in places. Edema is observed in the foci of the greatest inflammation. In hyperplastic forms, the thickening of the mucous membrane is more pronounced than in previous forms. Pathological changes are predominantly proliferative in nature due to the growth of connective tissue elements of the proper layer of the mucous membrane. The formation of granulation tissue and polyps is noted. The development of connective tissue in some areas can be combined with sclerosis and thickening of the mucous membrane in other places. The inflammatory process extends to all its layers, capturing in some cases the periosteal layer. This leads to periostitis, and with an unfavorable development of the process, to osteomyelitis. Due to the development of sclerosis of the mucous membrane and the delay in resorptive processes in case of bone disease, the formation of pseudocholesteatoma is possible, which is a thickened mucus without cholesterol inclusions and with a large number of leukocytes, as well as colonies of putrefactive microbes. The accumulation of pseudocholesteatoma and caseous masses and the pressure exerted by them on the walls of the paranasal sinuses lead to bone resorption and the formation of fistulas. It has now been established that such forms of sinusitis can also develop as a result of fungal infections of the sinuses. A special place is occupied by allergic forms of sinusitis, which are combined with similar processes in the nasal cavity and are called allergic rhinosinusitis (rhinosinusopathy). This form is characterized by the appearance in the sinuses (especially in the maxillary) formations of a rounded shape. They are localized swelling of the mucosa and are often incorrectly referred to as cysts. In these cases, during the puncture of the maxillary sinus, the needle pierces this cyst-like formation, and an amber-colored serous fluid is poured into the syringe, and the bladder walls collapse. The fundamental difference between such a pseudocyst and a true cyst of odontogenic origin is that it has only an outer epithelial lining formed by the sinus mucosa. The pseudocyst cavity is formed as a result of the splitting of its own layer of the mucous membrane by the transudate accumulating in its thickness. A true cyst of odontogenic origin also has an inner epithelial membrane emanating from the periodontium. The size of the pseudocyst (allergic mucosal edema) may change under the influence of hyposensitizing therapy and the appointment of glucocorticoids. On radiographs (better tomograms), in cases of odontogenic cysts, a thin, partially resorbed bone layer can be seen contouring the cyst. It is formed as a result of displacement of the lower wall of the maxillary sinus by a developing cyst. Clinical symptoms in chronic sinusitis outside the stage of exacerbation are less pronounced than in acute ones. In some patients, a decrease in working capacity is possible. The nature of the symptoms and their severity largely depend on the form of sinusitis, the localization of the process and its prevalence. Headache in chronic sinusitis is less severe, it may be indefinite. However, in some cases, patients accurately localize the pain in the area of the affected sinus. Nasal congestion is usually moderate, more pronounced in allergic polyposis and fungal forms of sinusitis, which is associated with similar lesions of the nasal mucosa. Often, patients note a violation of the sense of smell. The nature of nasal discharge also depends on the form of sinusitis. With fungal infections, they have certain characteristic differences. So, with mold mycosis, the discharge is usually viscous, sometimes jelly-like, has a whitish-gray or yellowish color. With aspergillosis, the discharge is gray, blackish blotches are possible, which can be thick, resembling cholesteatoma masses. With candidiasis, the discharge is similar to a whitish curd mass. With fungal sinusitis, neurological pain in the area of the affected sinus is often noted. More often than with other forms of sinusitis, there is swelling of the soft tissues of the face, usually in the region of the maxillary sinus. With exacerbation of chronic sinusitis, the clinical picture resembles an acute process of damage to one or another paranasal sinus and often depends on the presence or absence of complications. It is necessary to pay attention to the ability of chronic sinusitis to proceed in an inexpressive latent form, when the clinical symptoms are not clear enough. This state indicates the presence of a certain balance in the development of the pathological process - the balance between the organism and the disease. Causing overstrain and depletion of immune mechanisms, it leads, as a rule, to the development of certain (often very serious) complications. The diagnosis of chronic sinusitis and variants of its manifestations are established on the basis of clinical and radiological data. X-ray, as well as CT and MRI studies are the most important diagnostic methods for identifying various forms of chronic sinusitis. They are supplemented by punctures (trepanopunctures) of the sinuses and laboratory studies (bacteriological, mycological, histological, etc.) of the contents obtained. In the diagnosis of chronic sinusitis, the most difficult is to identify inflammation of the sphenoid sinus - chronic sphenoiditis. The sphenoid sinus, located in the deep parts of the base of the skull, is known in the literature as the "forgotten sinus", the diagnosis of diseases of which requires experience and skill. The close attachment of the sphenoid sinus to the diencephalic and other vital structures of the brain and visual pathways determines its clinical significance and the appearance of various neurological and asthenovegetative disorders. The symptoms of chronic sphenoiditis are varied and vague. In patients, sleep disturbance, loss of appetite, memory impairment, dizziness, the appearance of paresthesia, persistent subfebrile condition, and sugar metabolism disorders are possible. Cases of development in some patients of a severe hypochondriacal condition requiring urgent neurological care are described. Damage to the cranial nerves (olfactory, optic, abducens), development of cavernous sinus thrombosis, and involvement of the meninges are a common complication of chronic sphenoiditis. Patients usually have a bilateral process. In 70% of cases, along with the defeat of the sphenoid sinus, other paranasal sinuses are also involved in the inflammatory process, polysinusitis develops. Most often, along with the sphenoid sinuses, cells of the ethmoid labyrinth (usually posterior) and maxillary sinuses are subject to inflammation (A. S. Kiselev, T. A. Lushnikova, 1994). Involvement of other paranasal sinuses in the inflammatory process often reduces the severity of individual clinical manifestations of sphenoiditis and complicates its diagnosis. However, despite the diversity of the clinical picture of chronic sphenoiditis, a targeted study can reveal three of its characteristic symptoms: headache, runoff of purulent discharge along the nasopharynx and posterior pharyngeal wall, as well as a subjective unpleasant odor felt only by the patient. Headache is the main symptom of chronic sphenoiditis. Its main distinguishing feature is the projection of a permanent place, resulting from irradiation to one or another place of the head. Most often, pain radiates to the parietal, occipital region and orbit. A feature of sphenoidal pains is their excruciating. There are sensations of squeezing the head with a hoop or finding it, as it were, in a vise. With irradiation of pain in the orbit, patients experience a feeling that is described as tearing out or indentation of the eyeball. Headaches are persistent, depriving a person of rest, sleep, they reduce memory, performance and interest in life. In some cases, they lead the patient to a state of stupefaction, the development of depression and anxiety. There is another feature of headaches in chronic sphenoiditis - this is their appearance or intensification when the patient is in the sun or in a hot room. Also characteristic is the appearance or intensification of headaches at night, approximately at 2-3 o'clock in the morning. This is probably due to the drying of the crusts of purulent secretion and blockage of the sinus outlet. With the free discharge of purulent discharge, headaches may not bother the patient, however, there may be complaints about the flow of purulent sputum along the back of the throat and the need for frequent spitting. This is observed with the so-called open sphenoiditis. On the contrary, if the outflow of pathological contents from the sinus is difficult (with the so-called closed sphenoiditis), the headache can be unbearable. The given information about the features of headaches in sphenoiditis allows us to consider them as a sphenoidal pain syndrome. The establishment of the pain syndrome determines the further sequence of targeted diagnostic studies. They include the identification of symptoms associated with the consequences caused by the discharge of purulent secretions from the sphenoid sinus. These secondary reactive changes in the mucous membrane of the deep parts of the nose, nasopharynx and posterior pharyngeal wall can be considered as a sphenoidal syndrome of the mucous membrane (A. S. Kiselev, V. F. Melnik, 1993). The third characteristic symptom of chronic sphenoiditis is a subjective sensation of an unpleasant odor resembling burnt paper. The appearance of the smell is caused by the fact that the purulent discharge stagnates and decomposes due to poor outflow, and the sphenoid sinus outlet opens into the area in close proximity to the olfactory fissure. The next step in the study of patients with suspected sphenoiditis is to conduct an x-ray examination of the paranasal sinuses, in which the sphenoid sinuses become the main object of attention. As the final stage of the diagnostic examination, diagnostic probing of the sinus through the natural fistula can be performed. If it is impossible to carry it out due to the anatomical features of the nasal cavity, preliminary operations are resorted to (elimination of the curvature of the nasal septum, conchotomy). If, for one reason or another, probing of the sinus fails, it is punctured. The anatomical landmark for probing and puncture is the Zuckerkandl line. It starts from the anterior nasal spine at the lower edge of the pyriform opening in the vestibule of the nose and passes through the middle of the middle nasal concha to the middle of the anterior wall of the sphenoid sinus. The angle between the floor of the nasal cavity and the Zuckerkandl line is about 30°. The distance from the nasal spine to the anterior wall of the sphenoid sinus is 6-8,5 cm and only in rare cases is more. During manipulation, a steeper direction of the instrument (there is a risk of damage to the sieve plate) and the use of force should be avoided. Signs of the probe getting into the sinus through the exit hole (or bent at the tip of the needle by perforating the front wall of the sinus) are the feeling of falling into the cavity and the impossibility of vertical displacement of the instrument, which seems to be fixed and does not fall down when it is no longer held (Grunwald's sign). The presence of pus or mucus during suction with a syringe or their appearance in the washing liquid during the washing of the sinus with an isotonic solution indicates an inflammatory process. It should be noted that carrying out the described diagnostic procedures requires a good orientation in the deep parts of the nose and a high manipulation technique from the doctor. Treatment The tactics of treating chronic sinusitis is determined by the clinical form of the disease. With exacerbation of chronic sinusitis, its exudative forms (catarrhal, serous, purulent) are usually treated conservatively. In this case, the same means and methods of treatment are used that are used in the treatment of acute sinusitis. Productive forms of chronic sinusitis (polypous, polypous-purulent) are treated promptly. Regardless of the form of chronic sinusitis, in the presence of visual and intracranial complications, the main method should be surgical treatment. With polypous sinusitis, combined with nasal polyposis, a preliminary nasal polypotomy is indicated, which is carried out using a polyp loop. It should be borne in mind that when removing polyps emanating from the olfactory region, olfactory filaments may break and the olfactory bulbs may detach from their branches passing through the sieve plate, which leads to anosmia. Surgical interventions on the paranasal sinuses. The main goal of surgical treatment for chronic sinusitis is to organize conditions for restoring the normal function of the affected paranasal sinus. To do this, regardless of the option of operative access to the sinus or to a group of sinuses (with polysinusotomy), a disturbed sinus anastomosis with the nasal cavity is created anew or restored, providing its free drainage and ventilation. To date, there are a large number of options for surgical interventions on the paranasal sinuses proposed for the treatment of sinusitis. All of them, depending on the approach, are divided into extranasal and endonasal. The nature of anesthesia during operations on the sinuses depends on the age of the patient, his general condition, the presence of concomitant diseases, complications and the volume of surgical intervention. Anesthesia can be local or general. To prevent possible complications, especially after extended surgical interventions on the paranasal sinuses (polysinusotomy), broad-spectrum antibiotics are prescribed for 5-6 days in the postoperative period, often in combination with sulfonamides and nystatin, desensitizing and sedative drugs. In some cases, it is advisable to use Trichopolum or Metagil - drugs that have an etiotropic effect on the anaerobic flora. After removing the tampons, to normalize the pH of the nasal cavity for 2-3 days, it is advisable to use an alkaline ointment, which is necessary to quickly restore the function of the mucociliary apparatus. In the postoperative period, the sphenoid sinus (as well as other opened sinuses) is washed through a cannula with a warm isotonic or furatsilin (1:5000) solution. Lecture No. 15. Rhinogenic orbital and intracranial complications The proximity of the nose and paranasal sinuses to the orbit and cranial cavity determines the possibility of developing rhinogenic orbital and intracranial complications. Ways of spread of infection: 1) contact route: through defects in the bone walls as a result of osteomyelitis or through congenital bone defects in the cerebral and orbital walls bordering the sinuses, as well as in the optic nerve canals (so-called dehiscence); hematogenous route (through veins and perivascular spaces); 2) lymphogenous pathway (including along the perineural fissures). 1. Orbital complications ClassificationThere are the following types of complications: 1) reactive edema of the tissue of the orbit and eyelids; 2) diffuse non-purulent inflammation of the tissue of the orbit and eyelids; 3) periostitis (osteoperiostitis); 4) subperiosteal abscess; 5) eyelid abscess; 6) fistulas of the eyelids and orbital wall; 7) retrobulbar abscess; 8) phlegmon of the orbit; 9) thrombosis of the veins of the ophthalmic tissue. In addition, such nosological forms as optic neuritis, retrobulbar neuritis and optochiasmal arachnoiditis can be added to this classification, representing, in essence, different stages of one disease. Visual disturbances can also be caused by cyst-like or air distension of the paranasal sinuses. Clinic Orbital complications and visual disturbances are manifested by general and local symptoms, the severity of which depends on the nature of the pathological process in a particular paranasal sinus, the type of complication and the localization of the focus in the orbit itself. The severity of the disease increases with the progression of the disease and the development of purulent variants of the orbital lesion - subperiosteal, retrobulbar abscess, orbital phlegmon. Reactive swelling of the tissue of the orbit and eyelids, as well as their diffuse non-purulent inflammation, especially often develops in childhood with acute ethmoiditis that occurs against the background of a respiratory infection. In this disease, swelling and redness of the skin in the eyelid area, narrowing of the palpebral fissure, hyperemia and edema of the conjunctiva, eyelids and eyeball are clinically noted. In cases of diffuse non-purulent inflammation of the tissue of the orbit and eyelids, chemosis (and even exophthalmos) can be observed with a displacement of the eyeball in one direction or another, depending on the location of the affected sinus. Treatment that improves the outflow of pathological contents from the paranasal sinuses quickly relieves the symptoms of this orbital complication. Periostitis (osteoperiostitis). There are simple (non-purulent) and purulent forms. Simple periostitis is clinically difficult to distinguish from reactive edema and diffuse non-purulent inflammation of the tissue of the orbit and eyelids. It is observed with catarrhal inflammation of the sinuses, purulent - with empyema. It is clinically manifested by inflammatory infiltration of tissues in the form of eyelid edema and injection of conjunctival vessels. The localization of painful swelling depends on the localization of the inflammatory process in the paranasal sinuses, with the elimination of which the clinical manifestations of periostitis quickly disappear. Purulent periostitis is more severe. It is characterized by a pronounced general reaction: high body temperature, general weakness, headache. Locally, on one of the walls of the orbit, a painful infiltrate is formed, in which the periosteum can detach from the bone with the formation of a subperiosteal (periorbital) abscess. The anatomical features of the structure of the tissues of the orbit determine the direction of the spread of pus, which, as a rule, does not occur inside the orbit, but outward, forming a purulent fistulous tract. The localization of a subperiosteal (periorbital) abscess becomes clear after the formation of a fistulous tract. With frontal sinusitis, such a spontaneous opening of the abscess occurs in the middle of the upper orbital margin or in the region of the upper inner corner of the orbit, above the internal ligament of the eyelids. A fistula can also be located there with inflammation of the ethmoid labyrinth, and with a disease of the maxillary sinus - in the lower orbital region. Subperiosteal abscess of the deep parts of the orbit is more severe. Such a complication occurs more often with purulent processes in the posterior lattice cells and the sphenoid sinus, as well as with a breakthrough of pus from the maxillary sinus through the posterior parts of its inner wall. In this case, the development of central scotomas, paresis of the abducens and oculomotor nerves, and the appearance of exophthalmos are possible. Subperiosteal abscess, which is a consequence of damage to the deep paranasal sinuses, may be complicated by retrobulbar abscess and phlegmon of the orbit. With a breakthrough of pus into the retrobulbar tissue and its subsequent limitation, a retrobulbar abscess develops. In the case of high virulence of microbes and a weakening of the body's resistance, the restriction of the abscess may not occur, and then the phlegmon of the orbit develops. Orbital phlegmon is the most severe and dangerous of all rhinosinusogenic orbital complications. Its development is always accompanied by a violent general reaction of the body: the body temperature rises significantly (up to 39-40 ° C), headache intensifies, nausea and vomiting may occur. Pain in the orbit increases, swelling and hyperemia of the eyes increase, chemosis becomes significantly pronounced. There is always exophthalmos with limited mobility of the eyeball. Perhaps the development of blindness due to impaired blood supply to the retina. Phlegmon of the orbit may be preceded by thrombosis of its veins, manifested by similar symptoms. Visual disturbances caused by cyst-like deformations (expansion) of the paranasal sinuses can manifest as a displacement of the eyeball. Cyst-like enlargements of the paranasal sinuses include mucocele and pyocele. The development of a cystic expansion of the sinuses is characterized by the closure of the anastomosis between the sinus and the nasal cavity, and therefore sterile mucus (mucocele) or pus containing low-virulent flora (pyocele) accumulates in it. A provoking factor in the development of this disease is an injury that disrupts the patency of the anastomosis of the sinus with the nasal cavity. The sinuses, which have narrow and long excretory channels and openings, are most often affected. The disease manifests itself in an increase in the volume of the affected sinus and a displacement of the eyeball, depending on the localization of the process. With damage to the frontal sinus, the eyeball shifts down and outward, with damage to the ethmoid labyrinth - outward and forward, and with damage to the sphenoid sinus - forward. Patients complain of a feeling of heaviness in the area of the affected sinus and orbit. In some cases, patients are only concerned about the increasing cosmetic defect. When the disease is localized in the area of the ethmoid bone, the function of the lacrimal ducts is disrupted, which is accompanied by lacrimation. Thinning of the bone walls caused by cystic expansion of the sinus is observed on palpation as a symptom of a parchment crunch. It is also possible the formation of defects in the bone walls of the cystically enlarged sinus. Then the sinus mucosa with its mucosal contents prolapses into the formed defect. It should be noted another reason for the cystic expansion of the paranasal sinuses, which can lead to visual impairment up to its complete loss - air expansion. This air enlargement of the sinus is not called a pneumocele, but a pneumatosinus. A pneumocele is an air tumor formed as a result of the accumulation of air in the cranial cavity in violation of the integrity of the walls of the pneumatic cavities (paranasal sinuses, mastoid cells), as a rule, occurs with fractures of the base of the skull. Pneumatosinus is characterized as an air expansion of any paranasal sinus with the absolute integrity of its bone walls. The triad of symptoms characteristic of the pneumatosinus of the sphenoid sinus: 1) increased pneumatization of the sphenoid sinus with the presence of an arcuate deformation of its upper wall, a bulge facing upwards, and its displacement in the cranial direction; 2) maintaining the airiness of the sinus; 3) progressive decrease in vision caused by atrophy of the optic nerves. Treatment Treatment of rhinogenic ophthalmic complications must be carried out in a hospital with the participation of otorhinolaryngologists and ophthalmologists, and in some cases with the involvement of other specialists. It should be comprehensive and often quite urgent, covering a wide range of activities depending on the nature of the lesion of the orbit and the pathological process in the paranasal sinuses. In case of non-purulent forms of orbital complications (such as reactive edema, diffuse non-purulent inflammation of the eye tissue) resulting from acute sinusitis, conservative treatment is carried out, which should include active sanitation of the paranasal sinuses through their effective drainage, antibiotic and antihistamine therapy. With the same complications, but developed as a result of exacerbation of chronic inflammation of the paranasal sinuses, conservative methods of treatment can be combined with sparing surgical intervention. In case of purulent processes in the orbit or in the presence of symptoms of visual impairment (in particular, with optic neuritis or with retrobulbar neuritis), regardless of the nature of the pathological process in the paranasal sinuses, a wide opening of the affected paranasal sinuses and simultaneous elimination of the purulent focus in the orbit are necessary. Treatment of mucocele and pyocele is surgical. With damage to the frontal sinus and the ethmoid labyrinth, both extranasal paraorbital and endonasal accesses are possible. The same lesion of the sphenoid sinus requires its opening by endonasal transseptal access for guaranteed sanitation. In case of atrophy of the optic nerves caused by the pneumatosinus of the sphenoid sinus, endonasal transseptal opening of the sphenoid sinus with careful curettage of the mucosa is also recommended. 2. Intracranial complications Intracranial rhinogenic complications are one of the most severe and dangerous consequences of diseases of the nose and paranasal sinuses. In etiology, respiratory viral infections play the main role, provoking exacerbation of chronic sinusitis and leading to a decrease in the reactivity of the body and activation of the secondary pathogenic flora. In most cases, complications develop as a result of exacerbation of chronic inflammation of the paranasal sinuses, and only 25% are the result of acute sinusitis. It should be added that many chronic paranasal sinusitis ending in intracranial complications occur in a latent, erased form, without pronounced clinical manifestations. Intracranial complications can be the result of gunshot and non-gunshot injuries of the nose and paranasal sinuses, and are also possible with suppurative processes in the area of the external nose (furuncle, carbuncle) and the nasal cavity (abscess of the nasal septum). The prognosis of rhinogenic intracranial complications is always serious. Currently, with the use of modern means, including timely adequate surgical intervention, active antibacterial therapy, as well as therapy that corrects hemodynamic, liquorodynamic and homeostatic disorders, mortality has significantly decreased (to 5-10%). Clinic, diagnosis and treatment In clinical practice, the following intracranial rhinogenic complications are of greatest importance: arachnoiditis, extra- and subdural brain abscess, sinus thrombosis of the cavernous and superior longitudinal sinus, meningitis and brain abscess. Rhinogenic arachnoiditis is much more common than it is diagnosed. It usually develops in patients suffering from sluggish latent sinusitis without distinct clinical symptoms. The defeat of the paranasal sinuses can be manifested by a slight parietal thickening of the mucous membrane or a slight decrease in transparency (the so-called x-ray sinusitis), as well as individual symptoms of rhinitis. In the development of arachnoiditis, along with an infectious onset, an essential role is played by the body's autosensitization to the decay products of the tissues of the brain and its membranes, which causes a proliferative nature and a sluggish, but progressive course of the inflammatory process. An important link in the pathogenesis of arachnoiditis is immune deficiency at the cellular and humoral levels. Pathological changes in arachnoiditis are defined as a proliferative-exudative process that captures the soft membranes of the brain, arachnoid, vascular and adjacent areas of the brain tissue. As a result, two main morphological variants of arachnoiditis (adhesive and cystic) develop, leading to a violation of the normal circulation of the cerebrospinal fluid, expressed to one degree or another. The clinical picture of arachnoiditis depends on the localization of the process and the degree of its prevalence. Basal rhinogenic arachnoiditis, localized in the anterior cranial fossa, proceeds without significant focal symptoms and therefore is not always recognized. Patients complain of constant headache in the forehead and bridge of the nose, which is accompanied by a feeling of slight dizziness, especially when tilting the head. The headache is aggravated by nasal congestion, coughing, prolonged physical, mental and visual stress, often when reading. A characteristic of basal rhinogenic arachnoiditis is the appearance of a sensation of pain in the eyes when the eyeballs are moved upward, which indicates reflex irritation of the meninges. With convergence of the eyes, slight weakness of the eye muscles on the side of the lesion can be detected, which is often the only objective neurological microsymptom of limited rhinogenic arachnoiditis. Localization of basal arachnoiditis in the region of the optic chiasm and chiasmal cistern of the brain leads to the development of optochiasmal arachnoiditis. Optochiasmal arachnoiditis is the most unfavorable variant of basal arachnoiditis. The clinical picture is dominated by visual disturbances. A progressive decrease in visual acuity is combined with a concentric narrowing of the visual fields, the appearance of cattle, often central, and a violation of color vision. This quickly leads to severe disability and social limitation of the diseased, among which young people of working age predominate. Visual impairment is often the only significant symptom. Oculomotor disorders may also develop, indicating involvement in the inflammatory process of III, IV and VI pairs of cranial nerves. Disseminated neurological microsymptomatics are also possible: mild headache, endocrine-metabolic disorders, sleep disturbance. Arachnoiditis of the convex surface of the brain is usually localized in the region of the Sylvian furrow. In his clinical picture, the main place is occupied by epileptic seizures, as well as mono- and hemiparesis. Arachnoiditis of the posterior cranial fossa is characterized by hypertensive syndrome, which is manifested by attacks of headache, vomiting, dizziness. Treatment of patients suffering from rhinogenic arachnoiditis should be comprehensive, including surgical debridement of all affected paranasal sinuses, as well as massive anti-inflammatory, hyposensitizing and dehydration therapy. Sanitizing surgery (polysinusotomy) is best done as early as possible, until irreversible atrophic changes in the optic nerve have developed. With rhinogenic arachnoiditis, clinical and radiological signs of sinusitis (polysinusitis) are usually insignificant. Extradural and subdural abscesses - limited purulent inflammation of the dura mater (limited pachymeningitis). Extradural abscess, as a rule, occurs when the infection spreads by contact as a result of osteoperiostitis and carious process in the wall of the paranasal sinuses, for example, in chronic frontal sinusitis, less often in ethmoiditis and sphenoiditis. Initially, there is inflammation of a limited area of the outer layer of the dura mater, which acquires a purulent or necrotic character. Gradually, with the development of the process, an abscess is formed, located between the bone and the dura mater, limited by adhesions and granulations. Depending on the localization of the purulent focus, an extradural abscess can be in the anterior (with frontal sinusitis and ethmoiditis) and in the middle (with sphenoiditis) cranial fossae. The main symptom of an extradural abscess is headache, which can be regarded as an exacerbation of sinusitis. Sometimes an extradural abscess is asymptomatic and is an incidental finding during surgery on the affected paranasal sinus, which is explained by the free emptying of the abscess through a fistula that opens into the sinus. If the emptying of the abscess is difficult, it gradually increases in size, which can lead to the appearance of symptoms characteristic of a volumetric process and associated with an increase in intracranial pressure: headache, nausea and vomiting unrelated to food intake, congestive optic nerve papilla on the side of the lesion, and also bradycardia. With an extradural abscess, a violation of the sense of smell is possible, as well as a violation of the function of the cranial nerves (abducent, facial, trigeminal, glossopharyngeal and vagus). As a result, a corresponding symptom complex arises: difficulty in retracting the eyeball outward, weakness of the facial muscles, weakening of the corneal reflex, paresis of the soft palate, manifested by choking and nasality. Subdural abscess occurs as a complication of acute or exacerbated chronic sinusitis. It can develop as a result of the spread of an extradural abscess through the dura mater or with hematogenous spread of the inflammatory process. The abscess formed in the subdural space is limited to a weak demarcation shaft, consisting of adhesions of the arachnoid, connective tissue and glial elements. The usual outcome of such an abscess, if untreated, is the spread of infection over the surface of the meninges with the development of diffuse leptomeningitis, or infection of the brain tissue with the development of an intracerebral abscess. A subdural abscess is not as asymptomatic as an extradural abscess. The severity of symptoms depends on the degree of barrierization of the process. Symptoms of increased intracranial pressure are accompanied by signs of damage to the meninges and brain matter. In patients with general malaise and a feverish state, there are noticeable changes in the hemogram (increased leukocytosis, a shift in the formula to the left, an increase in ESR). The pressure in the spinal space is moderately increased, in the cerebrospinal fluid, usually sterile, there is an increase in the amount of protein and cells, which indicates a local reactive inflammatory process and irritation of the meninges. Treatment of extra- and subdural abscesses is surgical. A wide opening of the affected paranasal sinuses is performed by external access to expose the dura mater within healthy tissues. The discovered abscess is drained. Active antibiotic therapy and other drug treatment is carried out, similar to the treatment of meningitis. Sinus thrombosis. The transition of the inflammatory process to the wall of the venous sinuses leads to the development of sinus phlebitis with their subsequent thrombosis. Among sinus thromboses of rhinogenic origin, the most frequent and dangerous is sinus thrombosis of the cavernous sinus. The cavernous sinus, as you know, is located above the body of the sphenoid bone and its sinus. It is a complex venous collector into which blood is drained from various venous sources. So, in front, the veins of the orbit flow into the cavernous sinus, anastomosing, in turn, with the veins of the face - frontal, supraorbital, angular and facial. The veins of the pterygoid plexus, ethmoid, pterygopalatine, pharyngeal plexus, posterior auricular and occipital veins also flow into this sinus. It communicates with the superior and inferior petrosal sinuses. The cavernous sinus borders on the internal carotid artery, abducens, trochlear and oculomotor nerves, as well as the first and second branches of the trigeminal nerve. It is the structure of the sinus that largely explains the clinic of its thrombosis. Sinus thrombosis of the cavernous sinus most often develops with furuncle and carbuncle of the nose, diseases of the sphenoid sinus and posterior ethmoid cells, as well as with intracranial complications. In most cases, thrombophlebitis of the cavernous sinus occurs secondarily, being a continuation of phlebitis of other venous vessels, most often the orbital and facial veins. However, it is possible to develop thrombophlebitis of the cavernous sinus as a result of the spread of otogenic infection along the stony sinuses. The development of thrombosis of the cavernous sinus is facilitated by its complex anatomical structure, a distinctive feature of which are numerous connective tissue bridges that slow down the movement of blood flow in the sinus. Sinus thrombosis is manifested by symptoms of a general septic nature: intermittent fever with tremendous chills and heavy sweats in the general extremely serious condition of the patient. The danger is getting into the small, and then into the systemic circulation of pieces of an infected blood clot. As a result, metastasis of the purulent process and the appearance of new purulent foci in various organs are possible. In addition to general septic symptoms, thrombosis of the cavernous sinus is characterized by local, ocular symptoms caused by impaired circulation of the ophthalmic veins. They can be bilateral, but are most pronounced on the side of the lesion. Eye symptoms are manifested by exophthalmos, swelling of the eyelids and conjunctiva in the form of increasing chemosis, loss of corneal reflexes. Due to the inflammatory focus of the orbital tissue and paresis of the oculomotor nerves, the movement of the eyeball becomes limited or impossible. Violation of the blood supply to the optic nerve and retina leads to optic neuritis and blindness. Stagnation can also be observed in the forehead and even the entire corresponding half of the face. A distinctive feature of sinus thrombosis from orbital phlegmon, which manifests itself with similar symptoms, is the absence of pain with pressure on the eyeball. With sinus thrombosis, bilateral changes in the tissues of the orbit are also possible as a result of the spread of thrombosis to the other half of the sinus. Often, thrombosis of the cavernous sinus is complicated by purulent meningitis, meningoencephalitis, brain abscess, which worsens the prognosis of the disease. Thrombosis of the superior longitudinal sinus is a much rarer complication. This venous sinus, like other intracranial sinuses, is formed by a duplication of the dura mater and, with its anterior section, borders on the posterior wall of the frontal sinus, the veins of which flow into this sinus. That is why thrombosis of the superior longitudinal sinus occurs most often with frontal sinusitis. The infection can penetrate not only hematogenously through the venous vessels of the sinus, but also by contact with osteoperiostitis of the posterior (cerebral) wall of the sinus. As with any sinus thrombosis, the disease of the superior longitudinal sinus is manifested by general septic symptoms. Of the cerebral symptoms, patients have headache, confusion or loss of consciousness, and there is a meningeal syndrome. Local signs of the disease are manifested by swelling of the soft tissues of the forehead and crown. Thrombosis of the superior longitudinal sinus, as well as thrombosis of the cavernous sinus, can be complicated by meningitis, meningoencephalitis, brain abscess, and cerebellar abscess, which complicates the diagnosis and exacerbates the prognosis of the disease. Treatment of sinus thrombosis requires not only antibiotic therapy and surgical sanitation of the affected paranasal sinuses, but also the active use of anticoagulants. In cases where sinus thrombosis has developed as a complication of a furuncle or carbuncle of the nose, they resort to ligation of the facial or angular veins. Antibiotics are administered intramuscularly, intravenously and intraarterially (preferably three types of antibiotics). For their endovascular administration, the superficial temporal artery and subclavian vein are usually catheterized. Lecture number 16. Acute inflammatory diseases of the pharynx 1. Acute pharyngitis Acute pharyngitis is an acute inflammation of the mucous membrane of all parts of the pharynx. This disease is more often concomitant with respiratory infections of viral and microbial etiology (influenza, adenovirus, coccal). The patient complains of a feeling of soreness or pain in the pharynx, perspiration, dryness, hoarseness, and on examination there is hyperemia of the mucosa of all parts of the pharynx, accumulation of viscous mucus on the back wall, sometimes of a hemorrhagic nature. General symptoms - weakness, fever, discomfort - are due to the underlying disease. For the treatment of acute pharyngitis, oil-balsamic drops in the nose are recommended, a mixture in equal amounts of sea buckthorn, vaseline and menthol oils 3-5 times a day, warm alkaline inhalations, lubrication of the pharyngeal mucosa with Lugol's solution on glycerin, analgesics, aspirin are prescribed orally. Differential diagnosis of acute pharyngitis is carried out with diphtheria, scarlet fever, measles, rubella and other infectious diseases. In acute pharyngitis, it is recommended to take a swab from the pharynx for corynobacteria, and if necessary, the patient is hospitalized in an infectious diseases hospital. 2. Angina Angina is an acute inflammation of the palatine tonsils and the mucous membrane of the pharynx. Angina according to clinical data and pharyngoscopic picture is divided into catarrhal, follicular, lacunar, ulcerative-membranous and necrotic. Angina is a common nonspecific infectious-allergic disease of predominantly streptococcal etiology, in which local inflammatory changes are most pronounced in the lymphadenoid tissue of the pharynx, most often in the palatine tonsils and regional lymph nodes. Manifested clinically in the form of catarrhal, follicular and lacunar tonsillitis. Nonspecific angina Nonspecific angina - catarrhal, when only the mucous membrane of the tonsils is affected, follicular - purulent damage to the follicles, lacunar - pus accumulates in the lacunae. It is usually caused by group A streptococcus. However, there is pneumococcal tonsillitis, staphylococcal tonsillitis and tonsillitis, in the etiology of which lies a mixed coccal flora. A variety of this angina is alimentary angina, caused by epidemic streptococcus. The microbe is introduced, as a rule, in case of violation of the cooking technology by unscrupulous workers. Catarrhal angina affects the mucous membrane of the tonsils and arches, while hyperemia of these parts of the pharynx is noted, but there are no raids. The patient notes pain when swallowing, burning in the pharynx. Has a bacterial or viral etiology. The temperature is subfebrile, fever is less common. Regional lymph nodes may be moderately enlarged. The disease lasts 3-5 days. Treatment - rinsing with soda, sage, lubricating the tonsils with iodine-glycerin, ingestion of aspirin. Catarrhal angina must be distinguished from acute pharyngitis, in which the entire mucous membrane of the pharynx is affected, especially its posterior wall. Follicular and lacunar tonsillitis are caused by the same pathogens and are similar both in clinical course and in the general reaction of the body and possible complications. The difference lies in the different form of raids on the tonsils. With follicular angina, suppuration of the follicles occurs, and dead white blood cells shine through the mucous membrane. With lacunar angina, inflammation begins with lacunae, where pus accumulates, then protruding from the lacunae to the surface of the tonsils. After 1-2 days, raids spread over the entire surface of the tonsils, and it is no longer possible to distinguish between two types of tonsillitis. Patients feel severe pain when swallowing, discomfort in the throat, refuse food. The cervical lymph nodes are sharply enlarged, the temperature rises to 39 and even 40 ° C. On the 2nd - 3rd day, a differential diagnosis is made with diphtheria. Already at the first examination, the patient must take a smear on a diphtheria bacillus, try to remove plaque with a cotton brush. If the plaque is removed, this speaks in favor of angina vulgaris, if it is difficult to remove, and bleeding erosion remains in its place, this is most likely diphtheria. In case of doubt, it is necessary to introduce antidiphtheria serum. Treatment of follicular and lacunar tonsillitis consists in rinsing the pharynx, a cervical semi-alcohol compress, prescribing analgesics, desensitizers (diphenhydramine, suprastin, tavegil), and broad-spectrum antibiotics intramuscularly. Patients are recommended a sparing diet. Angina, caused by adenoviruses, proceeds in the form of diffuse acute pharyngitis, although it can also be accompanied by raids on the tonsils. Typical for adenovirus infection is a widespread lesion of the lymph nodes and a very frequent combination with conjunctivitis. This is especially true for adenovirus type 3, which causes pharyngoconjunctival fever. A similar picture is given by the influenza virus, but in 10-12% of cases it can be combined with streptococcal tonsillitis. Acute inflammation of the tonsils of another localization. Angina of the lingual tonsil has characteristic symptoms - pain in the region of the deep pharynx, which increases sharply when you try to protrude the tongue. The diagnosis is made by indirect laryngoscopy using a laryngeal mirror. Angina of the nasopharyngeal tonsil. Pain is localized in the nasopharynx, a thick mucous discharge is released from the nose, an acute runny nose is noted. With posterior rhinoscopy, an edematous tonsil of a cyanotic color is visible, sometimes with raids, thick mucus flows down the back of the pharynx. Angina as a syndrome of common infectious diseases Angina with scarlet fever can proceed in different ways. Most often it is angina catarrhal and lacunar. In the classic course of scarlet fever, there is a characteristic redness of the soft palate in the circumference of the pharynx, which does not extend beyond the soft palate, swelling of the cervical lymphatic glands and a whitish thick coating on the tongue, followed by its cleansing when the tongue takes on a bright color. To make a diagnosis, it is necessary to take into account all the symptoms of the disease, especially the scarlatinal rash in the region of the mastoid process and flexor surfaces of the extremities. There are severe forms of scarlet fever, occurring in the form of: 1) pseudomembranous angina with the formation of a fibrinous exudate widespread on the mucous membrane of the tonsils, pharynx, nasopharynx and even cheeks in the form of a thick grayish film tightly soldered to the underlying tissue. There is a bright hyperemia of the pharyngeal circumference, a rash appears already on the first day of the disease. The prognosis of this form of scarlet fever is unfavorable; 2) ulcerative necrotic angina, characterized by the appearance of grayish spots on the mucous membrane, quickly turning into ulcers. There may be deep ulceration with the formation of persistent defects of the soft palate. Lateral cervical lymph nodes are affected by extensive inflammation; 3) gangrenous tonsillitis, which is rare. The process begins with the appearance of a dirty gray plaque on the tonsils, followed by deep tissue destruction up to the carotid arteries. Angina with diphtheria can occur in various clinical forms. With diphtheria, plaques go beyond the arches. For angina, the pathognomonic is the strict border of the distribution of raids within the tonsils. If raids spread beyond the arches, the doctor must question the diagnosis of nonspecific tonsillitis. There is a simple diagnostic test. The plaque is removed from the tonsil with a spatula and dissolved in a glass of cold water. If the water becomes cloudy, the plaque dissolves, then it is a sore throat. If the water remains clear, and plaque particles have surfaced, then this is diphtheria. Angina with measles proceeds under the mask of catarrh in the prodromal period and during the rash. In the second case, the diagnosis of measles does not cause difficulties; in the prodromal period, it is necessary to monitor the appearance of measles enanthema in the form of red spots on the mucous membrane of the hard palate, as well as Filatov-Koplik spots on the inner surface of the cheeks at the opening of the Stenon's duct. The course of sore throat with rubella measles is similar to measles. Angina with influenza proceeds in the same way as catarrhal, however, diffuse hyperemia captures the tonsils, arches, tongue, back wall of the pharynx. Erysipelas is a serious disease that often occurs along with facial erysipelas. It starts with a high temperature and is accompanied by severe pain when swallowing. The mucosa is colored bright red with sharply defined reddening borders, it seems varnished due to edema. Angina with tularemia begins acutely - with chills, general weakness, reddening of the face, enlargement of the spleen. For differential diagnosis, it is important to establish contact with rodents (water rats, house mice and gray voles) or blood-sucking insects (mosquitoes, horseflies, ticks). Angina with tularemia in most cases occurs when infected by the alimentary route - when drinking water, food after an incubation period of 6-8 days in an infected patient. Another differential diagnostic sign is the formation of buboes - packets of lymph nodes in the neck, sometimes reaching the size of a chicken egg. Lymph nodes may suppurate. The picture of the pharynx may resemble catarrhal or more often membranous angina, erroneously diagnosed as diphtheria. Angina with blood diseases Monocytic tonsillitis (infectious mononucleosis or Filatov's disease) can clinically proceed in a variety of ways - from catarrhal to ulcerative necrotic. The etiology of this disease has not been fully elucidated. Clinically: an increase in the liver and spleen (hepatolienal syndrome), the presence of compacted and painful to the touch lymph nodes (cervical, occipital, submandibular, axillary and inguinal, and even polylymphadenitis). A pathognomonic symptom is the appearance in the peripheral blood of atypical mononuclear cells. Agranulocytic angina is associated with the complete or almost complete disappearance of granulocytes in the peripheral blood with the preservation of monocytes and lymphocytes against the background of severe leukopenia. The etiology of the disease has not been elucidated, it is considered polyetiological. The disease is associated with the immoderate and uncontrolled use of drugs such as analgin, pyramidon, antipyrine, phenacytin, sulfonamides, antibiotics, chloramphenicol, Enap. The clinical picture is usually severe and consists of symptoms of acute sepsis and necrotic tonsillitis, since the microbes that inhabit the pharynx belong to the opportunistic flora and, when the leukocyte protection is turned off and other adverse circumstances, they become pathogenic and penetrate into the tissues and blood. The disease is severe, with high fever, stomatitis, gingivitis, esophagitis. The liver is enlarged. The diagnosis is made on the basis of a blood test: leukopenia is sharp, below 1000 leukocytes per 1 mm3 blood, absence of granulocytes. The prognosis is serious due to the development of sepsis, laryngeal edema, necrosis of the tissues of the pharynx with severe bleeding. Treatment consists of fighting a secondary infection - prescribing antibiotics, vitamins, throat care (rinsing, lubricating, irrigating with antiseptic, astringent, balsamic solutions), intravenous transfusion of leukocyte mass. The prognosis for this disease is quite serious. Alimentary-toxic aleukia is characterized by the fact that, unlike agranulocytosis, when only granulocytes (neutrophils, eosinophils) disappear from the peripheral blood, the disappearance concerns all forms of leukocytes. The disease is associated with the ingestion of a special fungus that multiplies in overwintered cereals left unharvested in the fields and contains a very toxic substance - poin, even a very small amount of which leads to contact lesions in the form of tissue necrosis, hemorrhagic ulcers affecting the entire gastrointestinal tract , and even getting feces on the buttocks causes their ulceration. The poison is heat-stable, so the heat treatment of flour (cooking baked goods, bread) does not reduce its toxicity. From the side of the pharynx, necrotic sore throat is pronounced, when the tonsils look like gray dirty rags, and a sharp, nauseating smell is released from the mouth. The number of leukocytes in the peripheral blood is up to 1000 or less, while granular leukocytes are completely absent. Characterized by high fever, the appearance of a hemorrhagic rash. Treatment at an early stage consists of gastric lavage, enemas, the appointment of a laxative, a sparing diet, intravenous infusions of saline with vitamins, hormones, glucose, blood transfusion, leukocyte mass. In the stage of angina and necrosis, antibiotics are prescribed. With sharp clinical manifestations of the disease, the prognosis is unfavorable. Angina in acute leukemia occur with varying degrees of severity, depending on the stage of leukemia. The onset of angina (usually catarrhal) proceeds relatively favorably, begins against the background of apparent well-being, and only a blood test allows us to suspect acute leukemia at this early stage of the disease, which once again proves the mandatory blood test for angina. Sore throats with developed leukemia, when the number of blood leukocytes reaches 20 or more, and the number of red blood cells drops to 000-1 million, sore throat is extremely severe in the form of an ulcerative-necrotic and gangrenous form with high fever and severe general condition. Nosebleeds, hemorrhages in organs and tissues, and enlargement of all lymph nodes occur. The prognosis is unfavorable, patients die within 2-1 years. Treatment of sore throat is symptomatic, local, antibiotics and vitamins are prescribed less often. Angina with infectious granulomas and specific pathogens Tuberculosis of the pharynx can occur in two forms - acute and chronic. In the acute form, hyperemia is characteristic with a thickening of the mucous membrane of the arches, soft palate, tongue, resembling a sore throat, body temperature can reach 38 ° C and above. There are sharp pains when swallowing, the appearance of gray tubercles on the mucous membrane, then their ulceration. A characteristic anamnesis, the presence of other forms of tuberculosis help in the diagnosis. Of the chronic forms of tuberculosis, it is more often ulcerative, developing from infiltrations, often proceeding without symptoms. The edges of the ulcer are raised above the surface, the bottom is covered with a gray coating, after its removal, juicy granulations are found. Most often, ulcers are observed on the back of the pharynx. The course of processes in the pharynx depends on many reasons: the general condition of the patient, his nutrition, regimen, social conditions, timely and correct treatment. In acute miliary form of tuberculosis, the prognosis is unfavorable, the process develops very quickly with a fatal outcome in 2-3 months. The treatment of tuberculosis of the pharynx, as well as its other forms, has become relatively successful after the advent of streptomycin, which is administered intramuscularly at 1 g per day for an average of 3 weeks. R-therapy sometimes gives good results. Syphilis of the throat. Primary syphilis most often affects the palatine tonsils. Hard chancre is usually painless. Usually, on a red limited background of the upper part of the tonsils, a solid infiltrate is formed, then erosion, turning into an ulcer, its surface has a cartilaginous density. There are enlarged cervical lymph nodes on the side of the lesion, painless on palpation. Primary syphilis develops slowly, over weeks, usually on one tonsil. The condition of patients with secondary angina worsens, fever, sharp pains appear. If syphilis is suspected, it is imperative to carry out the Wasserman reaction. Secondary syphilis appears 2-6 months after infection in the form of erythema, papules. Erythema in the pharynx captures the soft palate, arches, tonsils, lips, surface of the cheeks, tongue. The diagnosis of syphilis at this stage is difficult until the appearance of papules from a lentil grain to a bean, their surface is covered with a touch of greasy sheen, the circumference is hyperemic. Most often, papules are localized on the surface of the tonsils and on the arches. The tertiary period of syphilis manifests itself in the form of gumma, which usually occurs several years after the onset of the disease. More often, gummas are formed on the back of the pharynx and soft palate. First, limited infiltration appears against the background of bright hyperemia of the pharyngeal mucosa. Complaints during this period may be absent. With a further course, paresis of the soft palate occurs, food enters the nose. The course of tertiary syphilis is very variable, depending on the localization and rate of development of gumma, which can affect the bone walls of the facial skull, tongue, main vessels of the neck, causing profuse bleeding, grows into the middle ear. If syphilis is suspected, a consultation with a venereologist is required to clarify the diagnosis and prescribe rational treatment. Fusospirochetosis. The etiological factor is the symbiosis of the spindle-shaped rod and spirochete in the oral cavity. A characteristic manifestation of the disease is the appearance of erosions on the surface of the palatine tonsils, covered with a grayish, easily removable coating. In the initial stage of the disease, there are no subjective sensations, the ulcer progresses, and only after 2-3 weeks there are mild pains when swallowing, regional lymph nodes on the side of the lesion may increase. During pharyngoscopy during this period, a deep ulcer of the tonsil is found, covered with a gray fetid plaque, easily removed. General symptoms are usually not expressed. In differential diagnosis, it is necessary to exclude diphtheria, syphilis, tonsil cancer, blood diseases, for which a blood test, Wasserman reaction, and a diphtheria bacillus smear are done. Rarely, pharyngitis and stomatitis join the defeat of the tonsils, then the course of the disease becomes severe. Treatment consists in the use of rinsing with hydrogen peroxide, a 10% solution of berthollet salt, potassium permanganate. However, the best treatment is a plentiful lubrication of the ulcer with a 10% solution of copper sulphate 2 times a day. The beginning of ulcer healing is noted already on the third day, which, in turn, also serves as a differential diagnosis with syphilis, blood diseases. The prognosis for timely treatment is favorable. Candidomycosis of the pharynx is caused by yeast-like fungi, often in debilitated patients or after uncontrolled intake of large doses of antibiotics that cause dysbacteriosis in the pharynx and digestive tract. There are sore throats, fever, against the background of hyperemia of the mucous membrane of the pharynx, small white plaques appear with further extensive necrosis of the epithelium of the tonsils, arches, palate, posterior pharyngeal wall in the form of grayish plaques, after the removal of which erosion remains. It is necessary to differentiate the disease with diphtheria, fusospirochetosis, lesions in blood diseases. The diagnosis is made on the basis of microscopy of smear materials with a coating of yeast-like fungi. Treatment involves the mandatory cancellation of all antibiotics, irrigation of the pharynx with a weak soda solution, lubrication of lesions with Lugol's solution on glycerin. This disease must be distinguished from pharyngomycosis, in which sharp and hard spikes protruding to the surface are formed in the lacunae of the tonsils. Since there are no signs of inflammation of the surrounding tissues and subjective sensations, the disease may not be detected by the patient for a long time. Conservative treatment is ineffective. As a rule, it is necessary to remove the affected tonsils. Paratonsillar abscess Between the capsule of the tonsil and the pharyngeal fascia is paratonsillar tissue, and behind the pharyngeal fascia, laterally, is the fiber of the parapharyngeal space. These spaces are filled with fiber, the inflammation of which, and in the final stage - and abscess formation determine the clinic of the named disease. An abscess is most often caused by nonspecific flora as a result of a tonsillogenic spread of infection. The disease begins acutely, with the appearance of pain when swallowing, often on one side. Usually, a paratonsillar abscess occurs after suffering a sore throat during the recovery period. When examining the pharynx, there is a sharp swelling and hyperemia of the tissues around the tonsil (arches, soft palate, uvula), protrusion of the tonsil from the niche, displacement to the midline. An abscess is formed on average about 2 days. Common symptoms are weakness, fever, enlargement of the cervical lymph nodes on the side of the abscess. The classic triad of paratonsillar abscess was noted: profuse salivation, trismus of chewing muscles and open nasality (as a result of paralysis of the muscles of the palatine curtain). Combined treatment of abscesses is prescribed: antibiotics intramuscularly, taking into account pain when swallowing and forced starvation, aspirin, analgesics, a half-alcohol compress on the side of the neck (on the side of the abscess), antihistamines. Simultaneously, surgical treatment is carried out. There are abscesses anteroposterior (pus accumulates behind the anterior arch and soft palate near the upper pole of the tonsil), posterior (with accumulation of pus in the region of the posterior arch), external (accumulation of pus between the tonsil capsule and pharyngeal fascia). Anesthesia, as a rule, is local - lubrication of the mucous membrane with a 5% solution of cocaine or a 2% solution of dicaine. A napkin is wound around the scalpel in such a way that the tip protrudes no more than 2 mm, otherwise the main vessels of the carotid pool can be injured. An incision is made with an anterior abscess strictly in the sagittal plane at the middle of the distance from the posterior molar to the tongue, then a blunt probe or hemostatic clamp (Holsted) is inserted into the incision and the edges of the incision are separated for better emptying of the abscess. When the pus is removed, the patient's condition, as a rule, improves significantly. A day later, the edges of the incision are again bred with a clamp to remove the accumulated pus. In the same way, the posterior abscess is opened through the posterior arch. It is more difficult and dangerous to open an external abscess, which lies deeper and requires more caution due to the risk of injury to blood vessels. Help with this can be provided by a preliminary puncture with a syringe with a long needle, when, if pus is detected, the incision is made in the direction of the puncture. After any incision in the pharynx, furacilin is rinsed. Very rarely there is a retropharyngeal abscess - an accumulation of pus in the region of the posterior pharyngeal wall. In children, this is due to the presence of lymph nodes in the retropharyngeal space, in adults - as a continuation of the external paratonsillar abscess. Lecture number 17. Chronic diseases of the pharynx 1. Hypertrophy of the tonsils AdenoidsIn children, there is a tendency to hypertrophy of the tonsils of the pharynx, especially the nasopharyngeal (the so-called adenoids). During puberty, the tonsils usually atrophy, with the exception of the palatine tonsils. The clinic and symptoms of adenoids are due to their special location on the vault of the nasopharynx, therefore they impede or completely exclude nasal breathing, ventilation of the auditory tubes, disrupt the function of the pharynx, which has an extremely adverse effect on the overall development of the child's body. This condition is characterized by a change in facial features, an open mouth, thickening of the wings of the nose, abnormal development of the dental system, sleep disturbance, coughing fits, a tendency to tonsillitis, otitis media, and pneumonia. In addition to complaints, anamnesis, general examination, posterior rhinoscopy is necessary for the diagnosis, but it is difficult in children, especially younger ones. V. I. Voyachek suggested that if adenoids are suspected, an anterior rhinoscopy should be performed with preliminary anemization of the nasal mucosa (for example, with a solution of galazolin or naphthyzinum), while the adenoids are quite clearly visible, and when the patient pronounces the number "3", there is a movement of the soft palate to determine the lower limit adenoids. There is a palpation method for examining adenoids, while the doctor stands behind the sitting child, fixes the head with his left hand, pressing it to himself, and examines the nasopharynx with the index finger of his right hand. The amount of hypertrophy is determined by three degrees: 1) to the upper edge of the coulter - I degree; 2) to middle turbinates - II degree; 3) to the lower shells and below - III degree. Inspection of the pharynx, tonsils, and otoscopy are required to assess the function of the middle ear and the condition of the eardrum. Conservative treatment of adenoids with various oils, a 0,25% solution of silver nitrate, therapy with ultraviolet or laser rays rarely gives a lasting therapeutic effect. The adenotomy operation is more effective, especially with concomitant pathology of the ENT organs or lungs. It is most often performed under local application anesthesia by lubricating the nasopharynx with a special cotton brush on a probe - a cotton holder. An assistant holds the child, previously wrapped in sheets to secure the arms, on his lap. The surgeon presses the tongue with a spatula and carefully inserts the adenoid under the control of vision behind the soft palate into the nasopharynx, gently resting on the fornix, then removes the adenoids with a quick sliding circular movement of the adenoid. Then the pharynx is examined, dried with cotton balls, and sometimes fragments of adenoids hanging into the oropharynx are removed. As a rule, bleeding is minor and stops on its own, complications are rare. Hypertrophy of the palatine tonsils Hypertrophy of the palatine tonsils is less common in children. There are three degrees of hypertrophy depending on the narrowing of the pharynx: 1) narrowing by 1/3 - I degree; 2) narrowing by 2/3 - II degree; 3) tonsils are in contact along the midline - III degree. It is wrong to consider hypertrophy as a sign of chronic tonsillitis, however, enlarged tonsils, like normal ones, can be affected by a chronic process. Enlargement of the tonsils is accompanied by coughing, choking, nasal voice, increased gag reflex, and in combination with chronic tonsillitis - frequent tonsillitis. Treatment is operative. Under local anesthesia, parts of the tonsils protruding beyond the arches are cut off with a special tonsillotomy. There are practically no complications. 2. Chronic inflammatory diseases Chronic pharyngitisInflammation of the mucous membrane of the pharynx is sluggish, manifested by an intermittent sensation of pain, dryness and discomfort in the pharynx, and rapid fatigue of the voice. Often this happens when exposed to household and professional factors, including alcohol, smoking, air pollution with dust (especially cement), and caustic chemicals. The influence of radioactive impurities in the air was also noted. A significant role in the genesis of this disease is played by the pathology of the nose - sinusitis, rhinitis, profuse purulent or mucous discharge. When examining the pharynx, flaccid hyperemia, moderate dryness of the mucous membrane are noted, on the back wall - often thick mucus. Hypertrophic pharyngitis is characterized by an increase in granules on the back of the pharynx to the size of a lentil grain (granular pharyngitis) or lateral ridges (lateral pharyngitis). atrophic pharyngitis. The mucous membrane of the pharynx is pale, thinned, looks like varnished, palatine tonsils, as a rule, are also atrophic. The etiology of this disease has not been fully elucidated, however, this fairly common disease occurs in more than 20% of women and 5-8% of men. It is manifested by constant dryness in the throat, perspiration, rarely pain, rapid fatigue of the voice during exercise, especially in singers, actors, lecturers, and teachers. Chronic tonsillitis Chronic tonsillitis is a chronic inflammation of the palatine tonsils; if other tonsils are affected, localization is indicated - chronic adenoiditis, tonsillitis of the lingual tonsil. According to the classification, two forms of chronic tonsillitis are distinguished: compensated and decompensated. The tonsils provide both local and general immune responses, especially in children. It is noted that children with removed tonsils are more likely to suffer from infectious diseases. Objective symptoms are of a non-permanent nature: soldering of the arches with the tonsils, their swelling, thickening, hyperemia. Two symptoms are more reliable - the presence of caseous plugs in the lacunae and an increase in regional (anterior cervical) lymph nodes. Exacerbation of chronic tonsillitis always proceeds in the form of a sore throat. The age of patients with chronic tonsillitis is practically unlimited, the same number of men and women are ill. Conservative treatment: antibiotics, sulfonamides, desensitizing drugs, inhalation, hormonal therapy, special mixtures (mephiditis, anginol), washing the lacunae of the tonsils with a thin cannula on a syringe with saline or an antibiotic, irradiating the tonsils with ultraviolet rays (the so-called tube quartz), laser irradiation of the tonsils. These methods do not give a lasting effect, so the main method of treating chronic tonsillitis is surgical - tonsillectomy. Tonsillectomy is performed mainly under local, less often under general anesthesia. The arches of one of the tonsils, the back wall of the pharynx, the root of the tongue are lubricated with a 2% solution of dicaine or a 5% solution of cocaine, then in the region of the anterior arch along the transitional fold, three injections are made with a 1% solution of novocaine at the poles of the tonsils and in the middle between them , lateral to the tonsil capsule into the paratonsillar space. Under this condition, further separation of the tonsil will take place with the least difficulty. The incision is made with a scalpel along the transitional fold at the upper pole, then the upper pole is detached with a special raspator, separated from the arches and separated with a capsule in the paratonsillar space. The lower pole is cut off with a special loop. Bleeding during the detachment of the tonsil and then stops with gauze and cotton balls, pressing them to the tonsil niche with a clamp. The other tonsil is then removed. After the operation, strict bed rest and hunger are necessary for XNUMX hours. Then the regimen is expanded by prescribing a sparing diet. After 5-7 days, the patient is discharged from the hospital for outpatient observation and release from work for 7-10 days. Complications from tonsillectomy are rare, except for bleeding from the tonsil niche - from 1,5 to 5%. It is stopped by pressing a cotton-gauze ball in the tonsil niche, applying a catgut suture to the vessel in the niche, or stitching the temples over the ball with a special needle, or balls with hydrogen peroxide, aminocaproic acid, or a hemostatic sponge. It should be noted that damage to the carotid arteries, retraction of a spatula or removed tonsil into the larynx lead to asphyxia. These complications require emergency care - ligation of the main vessels of the neck or laryngoscopy with removal of a foreign body in the larynx. Collapse and fainting of the patient are not uncommon during tonsillectomy, so patients must be examined by a general practitioner and anesthesiologist before surgery. In some cases, the operation has to be performed under endotracheal anesthesia. The technique of operation is the same. Lecture No. 18. Foreign bodies and damage to the pharynx. Anomalies in the development of the pharynx Foreign bodies, which are a variety of objects, enter the pharynx when breathing or swallowing. The outcomes of a foreign body in the pharynx are different: it can be coughed up, thrown out with exhalation, spit out, lie freely in the pharynx without injuring the mucous membrane, move further and become a foreign body of the larynx, trachea and bronchi, esophagus, finally, injure the mucous membrane and exit into soft tissues, most often the tonsils, piriform sinuses, the root of the tongue. Small piercing foreign bodies, such as thin fish bones, often pierce the palatine tonsils, are visible with pharyngoscopy, and are usually easily removed with forceps. It is more difficult when removing foreign bodies from the laryngopharynx using indirect laryngoscopy and laryngeal forceps, and if this fails, then with direct laryngoscopy. If the foreign body is injurious at the same time, then emphysema and edema of the prevertebral cellular space occur, then such a severe complication as mediastinitis may develop. In addition, as a result of edema, an overhang of the posterior pharyngeal wall occurs, making it difficult to examine the laryngopharynx and manipulate in this area. As a rule, the foreign bodies of the pharynx described above are safely removed without leading to death from acute asphyxia, like foreign bodies of the larynx. The exception is large foreign bodies that get stuck in the oropharynx during the act of swallowing, because they cannot slip into the esophagus from the epiglottis, which at this time closes the entrance to the larynx. If such a foreign body is not able to expectorate the patient with a strong exhalation or vomiting, loss of consciousness and death may occur. 1. Damage to the pharynx Wounds of the pharynx distinguish between internal and external. Internal injuries are associated, as a rule, with foreign bodies or random objects (more often in children). Tactics of treatment - removal of a foreign body, anti-inflammatory therapy, sparing diet. External injuries of the pharynx occur with incised, stab or gunshot wounds of the face and neck and differ in a variety of symptoms and degrees of severity depending on the location of the wound and the course of the wound channel, which determine damage to other organs of the neck, large vessels, and spine. In the diagnosis of damage to the pharynx, in addition to pharyngoscopy, external examination, radiography is of great importance for determining foreign bodies (such as a bullet, a fragment, a fragment of a cold weapon) and spinal injuries. Therapeutic measures must begin with stopping the bleeding. Here, tamponade of the nasopharynx can be successfully applied in case of bleeding from it or tamponade through the wound channel (as, for example, when the jugular vein is injured - between the lower jaw and the styloid process). If necessary, they also ligate the main vessels - the external and even the common carotid arteries. Another vital issue is the provision of respiratory function, which can be impaired both by the injury itself and its consequences (hematoma, edema, inflammation). Here, decongestant therapy can be applied, and if necessary, a tracheotomy. After hemostasis and restoration of breathing, it is necessary to treat neck wounds, remove damaging accessible foreign bodies. The patient's nutrition should also be provided by a doctor, since most often with such injuries, a probe is required to be inserted into the esophagus to prevent food and liquid from entering the wound canals for 1-2 weeks. 2. Anomalies in the development of the pharynx Anomalies in the development of the pharynx are quite rare, no more than 1% of all its diseases. First of all, this is the non-closure of the soft palate, which leads to a violation of the function of swallowing (the ingress of food and liquid into the nasopharynx and nasal cavity) and the function of speech (open nasality). On examination, a sagittal cleft of the soft palate is determined in the middle of it, often the tongue is absent or, conversely, bifurcated. The treatment of this anomaly is surgical - plastic surgery of the soft palate. Another developmental anomaly is associated with non-closure of the second branchial slit and the formation of a branching canal leading from the supra-myndaloid fossa into the depths of the soft palate. Such a channel is of some importance in the pathogenesis of paratonsillar abscesses. There are no other pathological manifestations of this anomaly. A similar anomaly with a wider canal in the form of a process extending into the thickness of the soft palate is also important in the development of abscesses. The third type of anomalies is associated with non-closure of embryonic canals and the possible formation of median and lateral fistulas (cysts) of the neck in adults. These canals originate in the pharynx and extend into the lower neck. Middle canal - from the root of the tongue through the body of the hyoid bone to the thyroid gland. It is non-fused and forms a median cyst of the neck. Another canal originates in the piriform sinus of the hypopharynx and descends along the sternocleidomastoid muscle, from which a lateral cyst of the neck may form. Both cysts can manifest themselves after an infection or neck injury, when a tumor-like formation appears, painless, mobile, gradually increasing in size. Further, it, as a rule, suppurates and is emptied through a fistula on the skin. This is repeated at regular intervals. Treatment of this pathology is surgical - removal of cysts of the neck, in the case of a median cyst, resection of the body of the hyoid bone is required, otherwise there may be relapses. Lecture No. 19. Diseases of the larynx. Foreign bodies of the larynx Objects that can be foreign bodies of the larynx are very diverse - from a fallen tooth and food items to small metal objects. They can lie freely or be introduced into the soft tissues of the larynx. There are differences in the clinic of foreign bodies depending on their localization. Foreign bodies of the upper floor of the larynx, including vestibular folds and blinking of the ventricle, mainly lead to mucosal edema, stenosis is rare here, only in the case of laryngeal angina. A foreign body located at the level of the glottis can lead to acute stenosis due to spasm of the vocal muscles and closing of the vocal folds. This is especially common in children, because they have a narrowing in the subglottic space and the foreign body cannot fall into the trachea, as in adults. The outcome of a foreign body of the larynx, as well as the pharynx, can be a natural rejection as a result of coughing, gagging, or a sharp exhalation, and, if necessary, with the help of indirect or direct laryngoscopy. In other cases, a foreign body is swallowed when it enters the esophagus or penetrates into the trachea, bronchi. In this case, death may occur as a result of asphyxia. If a foreign body has fallen into the trachea, then the immediate danger of asphyxia, as a rule, does not arise. The danger lies in the possible blockage of the pulmonary or lobar bronchi, followed by atelectasis of the lung. Foreign bodies of the trachea and bronchi are removed by tracheobronchoscopy. 1. Acute laryngitis Acute laryngitis is an inflammation of the mucous membrane of the larynx, which, as a rule, is affected a second time in acute respiratory infections, is less often an independent disease, while there is always inflammation of the mucous membrane of the trachea. In the first place are the defeat of the voice (dysphonia or aphonia), perspiration and burning in the larynx, cough, fever. On examination - hyperemia of the mucous membrane of the vocal folds, other parts of the larynx, sometimes - mucus in the folds. Dysphonia is explained by swelling of the mucous membrane of the folds, swelling of the tissues of the blinking ventricles, which disrupts the free oscillations of the folds. Aphonia occurs with paresis of the vocal muscle, the glottis does not close completely, taking an oval shape during phonation. With influenza, hemorrhagic laryngitis is observed when hemorrhages occur under the mucous membrane of the vocal folds. When conducting differential diagnosis, it is necessary to take into account the condition of the pharynx, since acute laryngitis in diphtheria, measles, scarlet fever is rarely isolated. The main method of treating acute laryngitis is inhalation: alkaline, alkaline-oil, inhalation with an individual inhaler (for example, Bioparox), according to indications, analgesics, antihistamines, vitamins are prescribed, and rarely antibiotics. Not bad help phonophoresis with hydrocortisone on the larynx or electrophoresis with potassium iodide, especially with aphonia. The infusion of various medicinal mixtures is also used with the help of a laryngeal syringe, which has a special long curved tip. For example, equal parts of sea buckthorn oil, menthol oil and an alkaline mixture for inhalation are taken. Before infusion, the mixture is emulsified by adding 1-1,5 ml of emulsion. Under the control of indirect laryngoscopy during phonation, the mixture is applied to the vocal folds. The prognosis is favorable. The duration of the disease is 7-10 days. Subglottic laryngitis (false croup). This type of acute laryngitis usually affects children. These features are explained by the structure of the larynx in children - the presence of loose fiber between the cricoid and thyroid cartilages outward from the mucous membrane of the larynx, which disappears with the growth of the larynx during puberty. This fiber is characterized by rapid (20-30 minutes) swelling with inflammation of the larynx, which occurs most often at night when the child is in a horizontal position. At the same time, the child wakes up in fear, rushes about, cries, stridor breathing appears, with a clear voice - a "barking" cough. When examining the larynx, there are, as it were, three floors of folds - vocal, vestibular, and below - swelling of the subglottic space in the form of third folds. During an attack of false croup, the child should be immediately picked up, giving him a vertical position, lower his legs into a hot bath (42-45 ° C), inhalation of a mixture of hydrocortisone and galazolin, mustard plaster on the chest, inside - antihistamines. Inspection of the pharynx and larynx is necessary, although laryngoscopy in children is extremely difficult and sometimes fails. By itself, false croup is not dangerous, an attack sometimes goes away even without treatment when the patient is in an upright position, it is dangerous not to recognize diphtheria and not to inject serum on time. Enlarged cervical lymph nodes, a hoarse voice, epidemiological data (contact with a patient with diphtheria, consultation of an infectious disease specialist) speak in favor of diphtheria. Throat angina (submucosal laryngitis). The disease is more often caused by vulgar flora with mechanical and thermal injuries, or with the transition of purulent processes from the tonsils, with pharyngeal processes. Laryngeal angina has three forms: such as inflammatory edema, laryngeal abscess, phlegmon of the larynx. With laryngeal edema, the general condition is slightly disturbed. With laryngoscopy, areas of vitreous edema are found, more often in the region of the epiglottis and (or) arytenoid cartilages. Swallowing is not difficult, moderately painful, breathing is free. However, with a sharp edema, there may be moderate disturbances in voice and breathing. Timely therapy gives a good effect. Recommended are aspirin, antihistamines, a warming compress on the neck, dehydration therapy, such as intravenous infusions (prednisolone - 30 mg, 5% ascorbic acid solution - 5 ml, panangin solution, saline - 400 ml, lasix - 1,5-2 ml ). The effect of treatment usually occurs quickly, the prognosis is favorable. However, in persons weakened, with reduced immunity, severe complications can occur. Abscess of the larynx. Symptoms are similar to the previous disease, but much more pronounced. With laryngoscopy, one can see not only the epiglottis and arytenoid cartilages, but also the spread of edema to the vallecules, piriform sinuses. Salivation and aphonia are noted due to severe pain in swallowing and voice formation. After 3-4 days from the onset of the disease, the formed abscess spontaneously opens, relief comes. Otherwise, the abscess is opened with a special laryngeal knife. Conservative treatment is the same as for edematous laryngitis. Phlegmon of the larynx is a very serious and relatively rare disease. The process covers the submucosal tissue of the entire larynx. Against the background of a sharp fever, swallowing disorder is observed due to unbearable pain. Respiratory problems come to the fore. With laryngoscopy, infiltration and hyperemia of all walls of the larynx are determined. In various places, purulent foci may open with the release of thick dark (hemorrhagic) pus. Fever occurs with a high temperature, it may be accompanied by dehydration due to the inability to swallow, therefore, such patients require parenteral nutrition and the introduction of saline solutions (for example, bisols, trisols). Due to the threat of asphyxia, an early tracheotomy is required. Anti-inflammatory treatment is intensive: large doses of modern antibiotics, hormones, antihistamines, analgesics. Fatal outcomes are rare, however, disability often occurs in the form of aphonia, cicatricial stenosis of the larynx, which then requires surgical interventions, since, along with other factors (specific infections, injuries, foreign bodies), phlegmon of the larynx can be the cause of chondroperichondritis of the cartilage of the larynx. Along with trauma (blunt, acute, gunshot), a frequent cause was a long stay in the larynx of the endotracheal tube (more than 3-5 days) for mechanical ventilation. The result is persistent stenosis of the larynx, requiring surgical treatment. 2. Chronic laryngitis The picture of chronic catarrhal laryngitis is similar to acute, but their symptoms can be smoothed out. They, as a rule, are combined with chronic pharyngitis, the course is undulating. Causes - chronic inflammatory diseases of the trachea, bronchi, lungs, sinusitis, vasomotor rhinitis, adverse environmental factors (frequent or constant cooling, impurities in the air, alcohol abuse). In 100% of smokers, the larynx is affected (smoker's laryngitis), but passive smoking (presence in a smoky room) is also quite harmful. Chronic laryngitis is expressed in persistent dysphonia, fatigue of the voice, its hoarseness, coarsening (the voice of a smoker). A kind of chronic laryngitis - atrophic, occurring with lakes, pharyngopathy; blanching and thinning of the mucous membrane are noted. Treatment is the same as for acute laryngitis, but preventive measures are of decisive importance: refusal of cold food and drink, bad habits, elimination of unfavorable factors of work and life, treatment of lung diseases. Hypertrophic laryngitis is diffuse and (more often) limited. When diffuse, the vocal folds are not only enlarged, but also covered by enlarged vestibular folds, which close during phonation, forming a kind of voice timbre ("dog's voice"). Limited hypertrophic laryngitis is more common. 1) Singers' knots. Occurs with improper use of the voice, very often found in singers with an incorrectly delivered voice (hence the name), actors, lecturers, teachers and anyone who overloads the vocal apparatus. There is an overgrowth of the epithelium and connective tissue on the border of the middle and posterior thirds of the vocal folds, no larger than a millet grain. The glottis does not close completely. 2) Pachydermia - limited outgrowths in the form of nodules and tubercles in the posterior parts of the vocal folds or in the interarytenoid space. 3) Subglottic laryngitis - a symmetrical thickening in the subglottic space (as with false croup) without signs of suffocation, but only with a change in the timbre and sonority of the voice. 4) Prolapse of the Morganian ventricle - it can be one- and two-sided, when a roller is visible between the vestibular and vocal folds, sometimes obscuring the latter for inspection. Prevention and treatment are the same as for the forms of chronic laryngitis described above. Myogenic and neurogenic paralysis of the larynx. The function of the muscles of the larynx can suffer from various infections, injuries, voice strain, congenital weakness. In the first place among myogenic paralysis is the paralysis of the internal vocal muscle. The folds do not close during phonation, an oval gap remains between them, which often happens in acute laryngitis. With damage to the lateral cricoarytenoid muscle, the anterior two-thirds of the glottis do not close, it looks like an irregular rhombus, and with paralysis of the interarytenoid muscles, they do not close in the posterior third of the glottis in the form of a triangle. With damage to the posterior vocalis muscle, which is the only dilator of the glottis, the vocal fold is motionless in the middle, the glottis expands only due to the opposite muscle. When breathing, the glottis has the shape of a right triangle. Voice formation and breathing, however, are not disturbed. With bilateral paralysis of these muscles, there is a threat of asphyxia and a tracheotomy is required. However, myogenic paralysis of these dilators of the glottis is very rare, usually due to damage to the recurrent nerve, the only one innervating this muscle, in contrast to the constrictor muscles that have cross-innervation. The main causes of damage to the recurrent (lower laryngeal) nerve are pathology of the aorta, hypertrophy of the heart muscle, tumors of the mediastinum. More often, the left recurrent nerve, which passes through the mediastinum much lower than the right, to the level of the aortic arch, is affected. 2,5-3% of strumectomies performed by surgeons are accompanied by unilateral, less often bilateral lesions of the recurrent nerve. With unilateral nerve damage, the fold is first located along the midline, then compensation of the respiratory function occurs due to the restructuring of the tone of the constrictors and the lateral shift of the affected fold by one third of the lumen. A healthy fold goes beyond the sagittal line during phonation, the arytenoid cartilage lies behind the paralyzed one. Unilateral lesion does not require treatment. With a bilateral lesion, as a rule, a tracheostomy is applied, and then an operation is performed on the larynx with the removal of one or two folds to eliminate stenosis (chordectomy). Stenosis of the larynx. Stenosis of the larynx and trachea lead to severe respiratory disorders (up to death from asphyxia). Laryngology studies only stenosis of the larynx and upper (cervical) trachea, while thoracic surgeons deal with stenosis of the thoracic region. There are differences in both pathogenesis and clinics of acute and chronic stenoses of the larynx. Acute stenoses occur most often as a result of edema of the fiber in the region of the vestibule of the larynx, the blinking sinus, and in children - in the subglottic space, less often - due to a foreign body. Laryngeal tonsillitis (submucosal laryngitis) is a disease in which swelling of the vestibule of the larynx begins very quickly, and this is where Voyachek's tonsil is located. Edema can grow very quickly: from several hours to 2-3 days and even lead to sudden asphyxia. False croup (subglottic laryngitis) occurs only in children, since they have a diameter of the inner half-ring of the thyroid cartilage much larger than a ring, and this space is filled with loose fiber. Edema develops here within 15-30 minutes, usually at night during sleep, when the child assumes a horizontal position. True croup - diphtheria of the larynx - is the second cause of stenosis - a foreign body of the larynx, since films are formed here as a result of necrosis of the mucous membrane, blocking the lumen of the larynx. There are also "external" foreign bodies that outwardly injure the mucous membrane with subsequent edema or penetrate into the lumen of the larynx and trachea, narrowing it. According to the existing classification, stenoses are divided into: 1) lightning-fast with complete closure of the glottis; 2) acute I, II and III degrees, depending on the narrowing of the glottis, respectively, up to one third of the lumen, no more than two thirds and more than two thirds of the lumen. Chronic stenosis of the larynx is not divided into degrees, because the patient's condition here largely depends on the compensation of the patient's respiratory function and adaptive mechanisms, their plasticity, therefore, with the same degree of stenosis, the condition of patients is very different. This can be clearly seen with stenosis of the trachea, when respiratory failure during exercise, shortness of breath of the patient, and sometimes the doctor, is explained by heart failure, increased blood pressure, stagnation in the pulmonary circulation, while in a patient, a mediastinal tumor already compresses the trachea to the diameter of a ball-bearing rod. pens, only a thorough X-ray examination reveals the true cause. In the etiology of chronic stenosis of the larynx and trachea are tumors of the larynx and trachea, trauma, infectious granulomas (scleroma, syphilis and tuberculosis of the larynx). With compensated chronic stenosis, tracheotomy is rarely done, only if an acute process is added, leading to edema and a significant narrowing of the glottis. A special type of stenosis of the larynx occurs as a result of paralysis of the vocal folds (unilateral or bilateral) due to damage to the lower laryngeal (recurrent) nerves, especially often occurs during strumectomy (in 2,5-4% of operated patients), which is explained by the passage of the recurrent nerve through the thyroid gland. Other causes of such a lesion are trauma, and the left recurrent nerve is syphilitic periortitis, since this nerve goes around the aortic arch. There are conservative and surgical treatment of stenosis. The first includes the treatment of the underlying disease and the stenosis itself, as a rule, the parenteral use of drugs: diuretics, antihistamines, hormones. With fulminant stenosis, a conicotomy is used - a horizontal dissection of the conical ligament connecting the thyroid and cricoid cartilages. It is easily felt on the neck, and when it is cut, there is no bleeding, since there are no muscles and blood vessels, while the surgeon enters the subglottic space. Fulminant stenosis occurs when the larynx is blocked either at the level of the laryngopharynx, where a large foreign body gets stuck during swallowing and fixes the epiglottis in the lower position (they say - the person choked), or (more often in children) the foreign body enters the glottis, there is a spasm of the vocal folds in middle position. When a foreign body threatening asphyxia falls into the trachea, stenosis, as a rule, does not occur, but there is a danger of blockage of the bronchi and lung atelectasis. Foreign bodies are removed with a bronchoscope. If with acute stenosis of the first degree, tracheotomy is done extremely rarely, then, on the contrary, with stenosis of the third degree, tracheotomy is absolutely indicated. Acute stenosis of the second degree requires a careful and balanced analysis to make a decision on tracheotomy, in order, on the one hand, to avoid unnecessary injury to a vital organ, and on the other hand, not to endanger the patient's life itself. Tracheotomy - the imposition of a stoma on the trachea in three classic places - between the 2nd and 3rd tracheal rings (upper), between the 3rd and 4th - middle, between the 5th and 6th - lower. In the first and third cases, the isthmus of the thyroid gland is displaced up or down, and in the second case, the isthmus is dissected. The technique of tracheotomy is simple - a skin incision is made from the edge of the thyroid cartilage down, not reaching the jugular notch. Then the anterior muscles of the neck are bluntly stratified, while it must be remembered that the stratification should be exactly along the midline. When approaching the trachea, the isthmus of the thyroid gland is determined, moved up or down, or crossed. The level of the tracheal incision is outlined. According to V. I. Voyachek, one of the ligaments between the cartilaginous rings of the trachea (transverse tracheotomy) is cut across, a tracheotomy tube is inserted here using a nasal mirror, the wound is not completely sutured in order to avoid emphysema of the neck tissue. The tube has a shield for fixing on the neck with gauze turundas, and a cotton-gauze napkin with a slot is placed under the shield. If necessary, the tube is drained by suction. The transverse incision of the trachea is the prevention of chondroperichondritis of cartilage rings. There is also a method of longitudinal section of two cartilages of the larynx (longitudinal tracheotomy) with the subsequent introduction of the tube. In this case, the development of perichondritis, prolonged non-healing of the stoma after removal of the tube, cannula-carrier, when adequate breathing is not provided without a tube, are possible. The choice of the method of tracheotomy according to Björk is unsuccessful, when a U-shaped window is applied with parallel incisions of the tracheal rings and the interannular ligament, followed by the abduction of the flap down and its fixation with sutures to the skin. Such an incision is made to exclude spontaneous prolapse of the tracheotomy tube and, in view of this, a new danger of suffocation. Such an incision leads to necrosis of the U-shaped flap of the trachea and the formation of persistent cicatricial stenosis with the need for further plastic surgery. Elimination of cicatricial stenosis of the larynx is a rather complex intervention, which has its own rules, possibilities and difficulties. 3. Damage to the larynx Injuries to the larynx are relatively rare. Distinguish between closed and open injuries, while closed are divided into internal and external. Internal injuries occur as a result of foreign bodies, medical manipulations (for example, tracheal intubation). Such injuries do not pose a particular danger, with the exception of the possibility of developing chondroperichondritis of the cartilage of the larynx, when the prognosis becomes serious. External closed injuries - bruises, compression of the larynx, fractures of cartilage, hyoid bone, tears of the larynx from the trachea. This can happen as a result of a blow to the larynx with hard objects, in a fight - with the edge of the palm. The victim often loses consciousness, shock occurs, local hemorrhages, subcutaneous emphysema, which can be superficial, and if it spreads into the laryngopharyngeal tissue, there is a danger of asphyxia, in such cases a tracheostomy is required. In addition to external examination, indirect laryngoscopy, radiography is of great importance in the diagnosis of larynx injury (not only for examining cartilage, but also for the spread of emphysema through internal cellular spaces). The prognosis for contusions of the larynx, especially with cartilage fractures, is always serious. The patient is in danger of strangulation not only due to stenosis of the larynx, but also possible tamponade of the trachea and bronchi with outflowing and gore blood, and in the following days mediastinitis may develop due to the penetration of infection there. Tracheotomy in such cases is necessary not only to restore breathing, but also to suck blood from the bronchial tree. Treatment of such patients is carried out exclusively in a hospital. If necessary, in case of significant crushing of the cartilage, a laryngofissure is performed to remove fragments, hemostasis. Patients are fed through a probe. There are three types of open injuries of the larynx - cut, stab and gunshot (bullet and shrapnel). Cut damage to the larynx occurs when the neck is cut, usually in a horizontal plane (from ear to ear), while depending on the height of the cut, the thyroid-hyoid membrane or conical ligament is cut. In the first case, the wound gapes, the laryngopharynx is clearly visible, breathing is not disturbed, and with a low cut, breathing may be disturbed due to blood flow. The death of the wounded comes quickly only in the case of cutting the carotid arteries. If this does not happen, the prognosis depends on the severity of inflammation from the larynx and surrounding tissues. Stab wounds of the neck with damage to the larynx are applied with thin, narrow, long objects and leave a narrow channel, which, when the injuring object is removed, is blocked along its length by the fascia of the neck (coulis syndrome), which contributes to the formation of emphysema and the development of mediastinitis, so such a channel has to be dissected. With neck injuries of any origin, especially with damage to blood vessels and nerves, shock develops, which also requires adequate therapy. Gunshot wounds of the larynx are most often combined, since other organs of the neck are also damaged. They are usually divided into through, blind and tangent. With penetrating wounds, a wounding projectile (bullet) pierces both walls of the larynx and goes beyond it, with a blind wound, the bullet remains in the cavity of the larynx, moving further either into the pharynx or into the trachea. With a tangential wound, the bullet only hits the wall of the trachea without tearing it. Medical measures are built in two stages - emergency care and subsequent rehabilitation. Emergency care includes providing breathing, stopping bleeding, treating a gunshot wound (if necessary, a laryngofissure), removing a foreign body (a wounding projectile), inserting a food probe. With a combined lesion, the participation of other specialists in the provision of emergency care is sometimes required (for example, a neurosurgeon, maxillofacial surgeon). The rehabilitation phase can be quite long, depending on the extent of the damage. Authors: Drozdov A.A., Drozdova M.V.
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