Inner ear injuries: causes, symptoms, diagnosis, treatment

Injuries to the inner ear are the cause of the emergence of the labyrinthine traumatic syndrome, which is a combination of specific signs of the disturbance of the functions of the sound and vestibular analyzers, combined with possible general and focal brain lesions. Labyrinth traumatic syndrome is divided into acute and chronic forms that arise with direct and indirect effects on the receptor formations of the ear maze of various traumatic factors. As a rule, contusions, injuries and explosive injuries of the Inside the ear are combined with similar brain damage and can be attributed to TBI with good reason. Labyrinthine traumatic syndrome is divided into acute and chronic syndromes.

Acute labyrinthine traumatic syndrome. Acute labyrinthine traumatic syndrome is a combination of signs of impairment of auditory and vestibular functions arising from the impact on the ear maze of traumatic factors of a mechanical or physical nature whose energy leads to the immediate disruption of the integrity of the traumatized structures at the anatomical or cellular, subcellular and molecular level.

Contusions of the ear maze. Under the contusion of the ear maze, a complex of injuries of its structures is understood with concussion, bruising, secondary compression of the anatomical formations of the inner ear, causing the occurrence of hypoxic edema or hemorrhage in them.

Pathogenesis. If the temporal region is bruised, mechanical energy is transferred to the ear maze directly through bone tissue and labyrinth fluids, and indirectly through brain tissue. In the latter case, the endolymphatic bag serves as the transferring link, to which a hydrodynamic wave propagating retrograde to the endolymphatic spaces of the ear maze is transmitted. Of all intracranial structures, the membranous and receptor formations of the inner ear are most sensitive to mechanical trauma, for the damage of which energy is required to be 100 times less than for the onset of a concussion of the mild brain. Often, signs of TBI mask acute cochleovestibular symptoms, which manifest only after the victim has emerged from the unconscious state.

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 an increase in venous pressure, hyperproduction of the cerebrospinal fluid, which ultimately leads to acute hydrocephalus and edema of the brain. Since the vessels of the ear maze are part of a single cerebral vascular system, basically the same pathoanatomical and functional abnormalities arise in them as in the vessels of the brain. In the case of a mechanical trauma to the ear maze, a circulatory disturbance occurs first, followed by changes in the production and chemical composition of the peri- and endolymph, a violation of their circulation and resorption. These phenomena increase the permeability of the hematolabyrinth barrier, disrupt the electrolyte balance, and lead to a dropsy of the labyrinth.

Pathological anatomy. Contusions of the ear maze are characterized by hemorrhages in the tissues and its fluid media, ruptures and detachments of its mobile elements (cover membrane of SpO, otolith and culvert apparatus, membranous ducts).

Symptoms are extremely characteristic. In the absence of violations of consciousness, the victim complains of severe dizziness, nausea, noise in one or both ears and in the head, the illusion of the movement of objects in sight. Of the objective symptoms characterized by spontaneous nystagmus, a violation of coordination tests, static and dynamic balance, hearing impairment, until its complete shutdown. The consequences of acute labyrinthine traumatic syndrome relate mainly to auditory function, which, depending on the severity of the lesion, can persist for a long time or even progress.

The diagnosis is made on the basis of anamnesis, the presence of characteristic subjective and objective symptoms. Particular attention is paid to the condition of the external auditory canal and tympanic membrane (the presence or absence of blood clots, ruptures, signs of ear lichorea). In the presence of adequate communication (spoken or written) of the victim with the doctor, in addition to the survey and examination, some functional tests are performed, by means of which the signs and the degree of lesion of the auditory and vestibular analyzers are established. All survey data having medical and legal significance are recorded in detail (logged). The degree of hearing impairment is determined by the study of "live" speech, the conduct of tokonotal tests (Weber and Schwabach tests), and threshold tonal audiometry. The state of the vestibular function is assessed by means of samples for spontaneous abnormal vestibular reactions and movement coordination tests. All the examination of the victim is carried out in a gentle mode, in a prone position. Provocative vestibular samples in the acute period of the labyrinthine traumatic syndrome are not performed. It is strictly forbidden to carry out a caloric test and ear flushing during bleeding from the external auditory canal.

Treatment of acute labyrinthine traumatic syndrome largely includes those that are performed by a neurologist with CCT, primarily measures aimed at preventing cerebral edema, disturbances of vital functions. In the presence of hemotimpanum, vasoconstrictive agents are prescribed in the nose to accelerate the evacuation of blood from the tympanum through the auditory tube. To prevent secondary infection prescribe per os sulfonamides and antibiotics.

Labyrinth disorders in fractures of the base of the skull. This type of TBI occurs when a person falls on the head or strikes a heavy object on the occipital or lateral surface of the head, sometimes when falling on the gluteal region or on the knees.

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

Longitudinal fractures account for 80% of all fractures of the pyramid. They arise with direct impacts on the temporomandibular region. The fracture line runs parallel to the large axis of the pyramid and captures the medial wall of the tympanum, in the area of which there are lateral sections of the ear maze and the horizontal part of the facial canal.

A transverse fracture occurs when the nape of the occipital and occipital parietal region of the skull strikes. It damages the ear maze and the external auditory canal, without touching the walls of the middle ear.

An oblique fracture occurs when an attack is made in the occipital-mastoid region and damages the inner ear, middle ear, facial canal and cavernous mastoid.

More rarely there are atypical fractures, the lines of which pass through zones of the least resistance of the skull base bones, as well as micro fractures and microcracks of the labyrinth bone capsule. Healing of bone tissue of the temporal bone occurs by forming a new bone tissue along the fracture line. In the bone labyrinth, because of the absence of the periosteum, the healing of the fracture occurs in a different way, namely, through the development of a fibrous tissue along the line of fracture, which is impregnated with calcium salts with the formation of dehydration. This process is especially characteristic for fractures in the area of the cape and labyrinthine windows, which under appropriate circumstances promotes penetration in the inner ear of the infection after a long time after trauma.

Symptoms depend on the severity of the CCT, which determines the cerebral and focal neurological symptoms, and the character of the fracture of the temporal bone. Early signs of a fracture of the pyramid are the paralysis of the facial and distracting nerves, which can be seen even in the comatose state of the victim. Paralysis of the facial nerve, which occurred immediately after the trauma, is a pathognomonic symptom of the fracture of the capsule of the ear maze. Paresis of the facial nerve, appearing a few minutes after the trauma and later, most often indicates the presence of a hematoma anywhere along the facial canal. If the fracture line of the base of the skull captures a round or oval window, then paresis occurs respectively in the second and third branches of the trigeminal nerve that exit through these openings from the cranial cavity. The appearance in 4-6 days in the region of the mastoid process of blue spots, which resulted from the penetration of hemolyzed blood from the deeper parts of the temporal bone, is also evidence of a fracture of the pyramid.

With longitudinal fractures of the pyramid, ruptures of the tympanic membrane are observed, in the absence of a rupture of the latter, blood can accumulate in the tympanic cavity, which shines through the tympanic membrane in a cyanotic-red color. With ruptures of the tympanic membrane and violation of the integrity of the solid meninges, the cerebral eurorrhea is observed. With longitudinal fractures, as a rule, the ear maze does not fall into the fracture line. With transverse and oblique fractures, both the cochlea and the labyrinth of the vestibular apparatus are destroyed, which causes complete disabling of the functions of these organs.

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

1. spontaneous recovery with some or other residual phenomena of cochlear and vestibular disorders;
2. the appearance of early neurological signs of nerve lesion of the scrotal fascicle;
3. the emergence of secondary infectious complications, caused by the penetration of infection to the cerebral membranes;
4. the occurrence of late neurological complications, caused by the consequences of organic lesions of the meninges and brain substance.

The most common causes of death are early complications in the form of coma, hyperthermia, cerebral edema, paralysis of the respiratory and vasomotor centers. Often bruises of the head lead to the appearance of extradural hematomas, caused by ruptured shell arteries. The presence of such a hematoma is indicated by the Gérard-Marchand symptom, a painful swelling in the temporal parietal region that arises from the rupture of the middle shell artery. Indications for trepanation of the skull at this stage are signs of increasing intracranial pressure: bradycardia, bradypnoea, increased blood pressure, mydriasis and progressive extinction of reflex activity.

Among late complications, the fracture of the temporal bone pyramid should be noted Eagleton syndrome, which occurs with an isolated increase in pressure in the posterior cranial fossa (hematoma): with a normal reaction from the lateral semicircular canal, the caloric stimulus of reaction to this stimulus from the other semicircular canals is absent or sharply reduced according to J. Portman (1956), the caloric nystagmus from each semicircular canal separately can be obtained by locating the head in such a way that the plane of the canal and coincided with the direction of the force of Earth's gravity).

The prognosis regarding the life of the patient and the secondary residual non-traumatic disorders is determined by the severity of the CCT. As for the prognosis for the auditory function, it is doubtful in the first hours and days after the trauma, in the future - cautious, because even in cases where the labyrinth and auditory nerve do not fall in the fracture line, a contusion injury can lead to a very short switch off of the auditory function. Later, months and years later, the surviving hearing may gradually fade due to atrophy of the auditory nerve and hair cells of the SpO. Vestibular function with integrity of the vestibular portion of the anterior-cochlear nerve and the corresponding receptor structures is restored to a greater or lesser degree after 2-3 weeks, and if damaged, after 1-2 months due to the contralateral labyrinth, however, the specific functions of the vestibular analyzer .

Treatment. Patients with fractures of the base of the skull and temporal bone are in particular placed in a neurosurgical or neurological hospital, but under certain circumstances they may be in the ENT department, where they should be treated accordingly. Strict bed rest for at least 3 weeks. With the development of traumatic shock and violations of respiratory and cardiac activity, caffeine, strophanthine, cordiamine, adrenaline, mezaton, lobelia, cititon, carbogen, etc. Are prescribed. To combat edema of the brain, dehydration agents (magnesium sulfate, sodium chloride, glucose, merkuzal, fonurit , hypothiazide, etc.).

[1], [2], [3]