Injuries to the inner ear: causes, symptoms, diagnosis, treatment

Inner ear injuries are the cause of labyrinthine traumatic syndrome, which is a set of specific signs of impaired functions of the sound and vestibular analyzers, combined with possible general and focal lesions of the brain. Labyrinthine traumatic syndrome is divided into acute and chronic forms, which occur with direct and indirect effects on the receptor formations of the ear labyrinth of various traumatic factors. As a rule, contusions, wounds and blast injuries of the inner ear are combined with similar damage to the brain and can rightfully be classified as TBI. Labyrinthine traumatic syndrome is divided into acute and chronic syndromes.

Acute labyrinthine traumatic syndrome. Acute labyrinthine traumatic syndrome is a set of signs of impairment of auditory and vestibular functions that arise when the ear labyrinth is exposed to traumatic factors of a mechanical or physical nature, the energy of which leads to immediate disruption of the integrity of the injured structures at the anatomical or cellular, subcellular and molecular level.

Contusions of the ear labyrinth. Contusion of the ear labyrinth is understood as a complex of damages to its structures due to concussion, bruising, secondary compression of the anatomical formations of the inner ear, causing the occurrence of hypoxic edema or hemorrhage in them.

Pathogenesis. In case of a contusion of the temporal region, mechanical energy is transmitted to the ear labyrinth directly through bone tissue and labyrinthine fluids, and also indirectly through brain tissue. In the latter case, the transmission link is the endolymphatic sac, to which a hydrodynamic wave is transmitted, propagating retrogradely to the endolymphatic spaces of the ear labyrinth. Of all the intracranial structures, the most sensitive to mechanical trauma are the membranous and receptor formations of the inner ear, the damage to which requires 100 times less energy than for the occurrence of a mild concussion. Often, signs of TBI mask acute cochleovestibular symptoms, which appear only after the victim comes out of unconsciousness.

As is known, the primary pathogenetic mechanism of TBI is the pathological reaction of the cerebral vessels, manifested by their paresis, increased permeability, hemorrhagic phenomena, venous stasis and increased venous pressure, hyperproduction of cerebrospinal fluid, which ultimately leads to acute hydrocephalus and cerebral edema. Since the vessels of the ear labyrinth are part of a single vascular brain system, they experience fundamentally the same pathological anatomical and functional disorders as the vessels of the brain. With mechanical trauma to the ear labyrinth, first of all, there is a circulatory disorder, then changes in the production and chemical composition of peri- and endolymph, disruption of their circulation and resorption occur. These phenomena increase the permeability of the hematolabyrinthine barrier, disrupt the electrolyte balance and lead to hydrocephalus.

Pathological anatomy. Contusion of the ear labyrinth is characterized by hemorrhages in the tissues and its liquid media, ruptures and tears of its mobile elements (the covering membrane of the SpO, the otolithic and cupular apparatus, the membranous ducts).

Symptoms are extremely characteristic. In the absence of disturbances of consciousness, the victim complains of severe dizziness, nausea, noise in one or both ears and in the head, illusion of movement of objects in the field of vision. Objective symptoms include spontaneous nystagmus, disturbance of coordination tests, static and dynamic balance, hearing impairment, up to its complete shutdown. The consequences of acute labyrinthine traumatic syndrome concern mainly the auditory function, which, depending on the severity of the lesion, can persist for a long time or even progress.

The diagnosis is established based on the anamnesis, the presence of characteristic subjective and objective symptoms. Particular attention is paid to the condition of the external auditory canal and the eardrum (the presence or absence of blood clots, ruptures, signs of ear lycorrhoea). If there is adequate communication (spoken or written) between the victim and the doctor, in addition to questioning and examination, some functional tests are carried out to establish the signs and degree of damage to the auditory and vestibular analyzers. All examination data that have medical and legal significance are recorded in detail (protocoled). The degree of hearing impairment is determined using a study of "live" speech, tuning fork tests (Weber and Schwabach tests) and threshold tonal audiometry. The state of the vestibular function is assessed using tests for spontaneous pathological vestibular reactions and tests for movement coordination. All examinations of the victim are carried out in a gentle mode, in a lying position. Provocative vestibular tests are not performed in the acute period of labyrinthine traumatic syndrome. It is strictly forbidden to perform a caloric test and ear lavage in case of bleeding from the external auditory canal.

Treatment of acute labyrinthine traumatic syndrome largely includes the same measures that a neurologist takes in case of TBI, primarily measures aimed at preventing cerebral edema and vital function disorders. In the presence of hemotympanum, vasoconstrictors are prescribed in the nose to accelerate the evacuation of blood from the tympanic cavity through the auditory tube. To prevent secondary infection, sulfonamides and antibiotics are prescribed per os.

Labyrinthine disorders in basal skull fractures. This type of TBI occurs when a person falls on the head or is hit with a heavy object on the occipital or lateral surface of the head, sometimes when falling on the buttocks or knees.

Pathological anatomy. Fractures of the skull base are most often localized in the middle cranial fossa on the lines connecting the outlet openings of the cranial nerves. The pyramid of the temporal bone is often involved in the fracture line, and then signs of labyrinthine traumatic syndrome arise. Fractures of the temporal bone are divided into longitudinal, transverse and oblique.

Longitudinal fractures account for 80% of all pyramid fractures. They occur with direct blows to the temporo-parietal region. The fracture line runs parallel to the major axis of the pyramid and includes the medial wall of the tympanic cavity, in the area of which are the lateral sections of the ear labyrinth and the horizontal part of the facial canal.

A transverse fracture occurs when there are blows to the occipital and occipito-parietal regions of the skull. It damages the ear labyrinth and the external auditory canal, without affecting the walls of the middle ear.

An oblique fracture occurs when a blow is applied to the occipito-mastoid region and damages the inner ear, middle ear, facial canal, and mastoid cavity.

Less common are atypical fractures, the lines of which pass through the zones of least resistance of the bones of the base of the skull, as well as microfractures and microcracks of the bony capsule of the labyrinth. The healing of the bone tissue of the temporal bone occurs through the formation of new bone tissue along the fracture line. In the bony labyrinth, due to the absence of the periosteum, the healing of the fracture occurs differently, namely through the development of fibrous tissue along the fracture line, which is impregnated with calcium salts with the formation of dehiscences. This process is especially characteristic of fractures in the area of the promontory and labyrinthine windows, which, under appropriate circumstances, contributes to the penetration of infection into the inner ear long after the injury.

Symptoms depend on the severity of the TBI, which causes general cerebral and focal neurological symptoms, and on the nature of the fracture of the temporal bone. Early signs of a pyramidal fracture are paralysis of the facial and abducens nerves, which can be noticed even in a comatose state of the victim. Facial nerve paralysis that occurs immediately after the injury is a pathognomonic symptom of a fracture of the capsule of the ear labyrinth. Facial nerve paresis, which appears a few minutes after the injury and later, most often indicates the presence of a hematoma somewhere along the facial canal. If the fracture line of the base of the skull covers the round or oval window, then paresis of the second and third branches of the trigeminal nerve, respectively, emerging from the cranial cavity through these openings, occurs. The appearance of blue spots in the mastoid process area after 4-6 days, caused by the penetration of hemolyzed blood from the deeper parts of the temporal bone, is also evidence of a pyramidal fracture.

In longitudinal fractures of the pyramid, ruptures of the eardrum are observed; in the absence of a rupture of the latter, blood may accumulate in the tympanic cavity, which shines through the eardrum as a bluish-red color. In case of ruptures of the eardrum and damage to the integrity of the dura mater, ear liquorrhea is observed. In longitudinal fractures, as a rule, the ear labyrinth does not fall into the fracture line. In transverse and oblique fractures, both the cochlea and the bony labyrinth of the vestibular apparatus are destroyed, which causes a complete shutdown of the function of these organs.

In case of a fracture of the temporal bone pyramid, several variants of the clinical course are described:

1. spontaneous recovery with some residual effects of cochlear and vestibular disorders;
2. the occurrence of early neurological signs of damage to the nerves of the auditory-facial bundle;
3. the occurrence of secondary infectious complications caused by the penetration of infection into the meninges;
4. the occurrence of late neurological complications caused by the consequences of organic lesions of the meninges and brain tissue.

Death is most often caused by early complications such as coma, hyperthermia, cerebral edema, and paralysis of the respiratory and vasomotor centers. Head injuries often result in extradural hematomas caused by ruptures of the meningeal arteries. The presence of such a hematoma is indicated by the Gerard-Marchand symptom - a painful swelling in the temporo-parietal region caused by a rupture of the middle meningeal artery. Indications for craniotomy at this stage are signs of increasing intracranial pressure: bradycardia, bradypnea, increasing arterial pressure, mydriasis, and progressive fading of reflex activity.

Among the late complications of a fracture of the pyramid of the temporal bone, it is necessary to note Eagleton's syndrome, which occurs with an isolated increase in pressure in the posterior cranial fossa (hematoma): with a normal reaction from the lateral semicircular canal to a caloric stimulus, the reactions to this stimulus from other semicircular canals are absent or sharply reduced (according to J. Portmann (1956), caloric nystagmus from each semicircular canal separately can be obtained by positioning the head in such a way that the plane of the canal under study coincides with the direction of action of gravity).

The prognosis for the patient's life and secondary residual noetraumatic disorders is determined by the severity of the TBI. As for the prognosis for the auditory function, it is questionable in the first hours and days after the injury, and cautious later on, since even in cases where the labyrinth and auditory nerve are not in the fracture line, contusion injury can lead to a very rapid shutdown of the auditory function. Later, after months and years, the remaining hearing can gradually fade due to atrophy of the auditory nerve and hair cells of the SpO. The vestibular function, with the integrity of the vestibular portion of the vestibulocochlear nerve and the corresponding receptor structures, is restored to some extent in 2-3 weeks, and if they are damaged - in 1-2 months due to the contralateral labyrinth, however, the insufficiency of the specific functions of the vestibular analyzer remains for years.

Treatment. Patients with fractures of the base of the skull and temporal bone in particular are placed in a neurosurgical or neurological hospital, however, under certain circumstances, they can also be in the ENT department, where they must undergo appropriate treatment. Strict bed rest for at least 3 weeks. In the development of traumatic shock and respiratory and cardiac disorders, caffeine, strophanthin, cordiamine, adrenaline, mesaton, lobelia, cytiton, carbogen, etc. are prescribed. To combat cerebral edema, dehydrating agents are used (magnesium sulfate, sodium chloride, glucose, mercusal, fonurit, hypothiazide, etc.).

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