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Labyrinthitis is an inflammatory disease of the inner ear. Most often, it is an otogenic complication of otitis media. Other forms are much less common. These include meningogenic and hematogenous labyrinthitis.

Meningogenic labyrinthitis occurs mainly in young children against the background of epidemic cerebrospinal meningitis. Infection from the subarachnoid space into the labyrinth extends through the cochlear's aqueduct or the auditory canal. Inflammation is purulent in nature and develops violently, which leads to sudden deafness (often in both ears). Vestibular symptoms are masked by manifestations of meningitis.

Hematogenous labyrinthitis occurs in infectious diseases (mumps, scarlet fever, measles, typhoid, etc.) and can be serous, purulent, and necrotic. Serous labyrinthitis develops more slowly than purulent meningogenic labyrinthitis. With the serous nature of the inflammation, complete suppression of the auditory and vestibular functions is not observed. Purulent and necrotic processes proceed unfavorably in the labyrinth. Necrosis occurs from the direct action of toxins and vascular thrombosis. Labyrinthitis in infectious diseases can develop against the background of secondary meningitis, as complications 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. The causative agents of otogenic labyrinthitis can be all types of polymorphic flora found in the middle ear with otitis media.

Pathogenesis. Labyrinthitis occurs against a background of a decrease in the general and local resistance of the body with high virulence of microflora.

In acute suppurative otitis media, a favorable factor for the development of labyrinthitis is the difficulty of 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 cochlea round window and the annular ligament of the stapes base swell and become permeable to toxins. A further delay in the evacuation of the discharge from the tympanic cavity can lead to melting of the membrane of the round window of the cochlea and penetration of pus into the perilymphatic space of the labyrinth.

Chronic purulent epithympanitis can lead to destruction of the labyrinth capsule in the area of ​​the protrusion of the lateral semicircular canal with the formation of a fistula in its bone wall. Channel fistula can also occur in patients previously operated on for chronic otitis media with inflammation in the postoperative cavity. Around the fistula, a protective granulation shaft is formed. Such a labyrinthitis for a long time is limited. Much less often with chronic suppurative otitis media, the labyrinth fistula occurs in the cape (promontorium) and the base of the stapes. 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 perilyme pressure due to the fact that the lining bone labyrinth endost swells and its dilated vessels become permeable to blood plasma. A small number of cellular elements appear in the perilymph, mainly lymphocytes, as well as fibrin. The development of serous-fibrinous inflammation sometimes leads to such an increase in the labyrinth pressure that the membrane of the round window of the cochlea breaks and the infection from the middle ear penetrates the labyrinth.

Purulent exudate consists of white blood cells (mainly neutrophilic). The inflammatory process goes to the membranous labyrinth, leading to the death of auditory and vestibular receptors.

Clinic. The clinical manifestations of otogenic labyrinthitis are composed of symptoms of impaired auditory and vestibular function and depend on its clinical form. Limited, induced, diffuse serous and diffuse purulent labyrinthitis are distinguished.

Limited labyrinthitis. The first symptom of limited labyrinthitis before the formation of the labyrinth fistula is dizziness, which occurs during sharp turns of the head and tilts of the body. In such patients, nystagmus may be detected. Hearing impairment cannot be entirely attributed to labyrinthitis, since chronic suppurative otitis media in itself causes severe hearing loss of a mixed nature. Limited labyrinthitis manifests as pressor nystagmus in the direction of the affected ear from the moment the lateral semicircular canal fistula is formed. It is detected during a tragal test or when the probe touches the fistula with cotton wool during the toilet of the ear and may be accompanied by dizziness, nausea. Sometimes a fistula, covered with granulations, is detected 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 the base of the stapes.

Induced labyrinthitis. With this form, the symptoms of maze irritation, manifested in spontaneous nystagmus towards the affected ear, dizziness and pathological autonomic reactions, are associated with the toxic effect of the products of acute purulent inflammation in the tympanum on the labyrinth through its windows. An inflammatory reaction in the labyrinth itself has not yet been observed. The sensorineural nature of hearing loss is also explained by the toxic effect. In addition to the toxic factor, a neuro-reflex mechanism of action on the labyrinth receptors is considered, as well as a change in their functional state as a result of collateral vascular edema.
The pathogenesis of induced labyrinthitis resembles the development of meningism in children from the difficulty of the outflow of pus from the tympanic cavity in acute otitis media. The phenomena of induced labyrinthitis, like meningism, disappear after unloading of 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 can occur after radical and auditory repair operations on the ear.

Serous diffuse labyrinthitis. With serous labyrinthitis, a decrease in hearing is observed in a mixed type with a predominant lesion in 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 accordingly directed first to the sick side, and then to the healthy side. Maze irritation phenomena can occur for several days. With the timely elimination of the inflammatory process in the middle ear, full or partial restoration of the auditory and vestibular functions of the maze is possible.

Purulent diffuse labyrinthitis is characterized by vivid clinical manifestations. Purulent inflammation in the maze quickly leads to the death of auditory and vestibular receptors.

The phase of the maze irritation is short-lived - several hours. During it, hearing deteriorates sharply and spontaneous nystagmus occurs in the direction of the affected ear. Marked dizziness, nausea and vomiting are noted. Due to dizziness and imbalance, patients take a horizontal position.

With the onset of the inhibition phase of the labyrinth, nystagmus changes its direction towards a healthy ear. Most often, it reaches the III degree. A harmonious reaction of the deviation of the hands and a miss with both hands towards the slow component of nystagmus is observed. When the intensity of nystagmus decreases to II, and then to I degree, the patient can already get up. When standing and walking, it also deviates toward the slow component of nystagmus. A characteristic sign of labyrinth ataxia is a change in the direction of body deflection with the head turned to the side. For example, if a patient deviates to the right, then when he turns his head to the left, he will deviate forward.

After the acute purulent process subsides, latent diffuse labyrinthitis can be observed. With a favorable outcome of the disease, the labyrinth subsequently grows through granulation with transformation into fibrous and bone tissue. With an adverse course of purulent labyrinthitis, labyrinthogenic purulent meningitis or cerebellar abscess may develop.

The death of the labyrinth is indicated by the lack of perception of a scream with muffling of the opposite ear with a Barani rattle and the negative result of a high-quality caloric test, which is carried out after the elimination of inflammatory phenomena in the labyrinth and tympanic cavity. Body temperature, in the absence of labyrinthogenic intracranial complications, is often subfebrile and even normal.

Treatment. With labyrinthitis, a comprehensive (surgical and conservative) treatment is performed.

Since otogenic labyrinthitis is a complication of acute or chronic purulent otitis media, then first of all they eliminate the purulent focus in the middle ear. 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. In the process of performing a radical operation, a thorough revision of the medial wall of the tympanum, attic, the area of ​​the protrusion of the lateral semicircular canal and labyrinth windows is carried out. If a labyrinth fistula is detected, gentle surgical treatment of its edges and plastic with a fascial, muscle or combined flap under a microscope is performed. For surgery on the middle ear, functional-friendly options are chosen.

The labyrinth is not opened, and drug treatment is carried out aimed at reducing the intralabyrinth pressure, preventing the transition of serous inflammation to purulent and the development of labyrinthogenic intracranial complications. Prescribe dehydration, antibacterial and detoxification agents. Antibiotics are administered in large doses, with purulent labyrinthitis - intravenously drip.

An indication for labyrinthotomy is a labyrinthogenic cerebellar abscess. In this case, the causative focus is removed and access to the abscess, which usually lies near the labyrinth, is facilitated. With labyrinthogenic meningitis, surgery on the middle ear with exposure of the dura mater of the cranial fossae is sufficient. Labyrinthotomy has to be performed with necrotic forms of labyrinthitis to remove sequestration and non-viable parts of the labyrinth capsule. The labyrinth is opened through the promontorium or posterior cranial fossa.

Prevention of otogenic labyrinthitis is the timely diagnosis and rational treatment of purulent diseases of the middle ear. In the presence of a labyrinth fistula, timely surgical intervention contributes to the preservation of hearing and the prevention of the transition of a limited labyrinthitis to the spilled one. In the presence of labyrinthine symptoms, patients with acute purulent otitis media and exacerbation of chronic otitis media urgently need to be sent to the hospital.
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