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Lecture notes, cheat sheets
Лор-заболевания. Болезни внутреннего уха. Лабиринтит. Отосклероз (конспект лекций)
Directory / Lecture notes, cheat sheets Table of contents (expand) 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. Authors: Drozdov A.A., Drozdova M.V. << Back: Mastoiditis. Adhesive otitis media >> Forward: Diseases of the inner ear. Meniere's disease. Sensorineural hearing loss
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