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Degenerative labyrinthotoxicoses: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 04.07.2025
 
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Neomycin selectively acts on the hair cells of the cochlea and often causes more frequent and profound hearing loss than streptomycin, up to and including complete deafness.

Quinine (quinine hydrochloride, quinine sulfate) causes cochleovestibular syndrome, similar in its manifestations to streptomycin toxic-degenerative labyrinthosis. Pathological changes occur in the vascular stria (vascular paresis, pathological changes in cells), in the external hair cells of the SpO, in the fibers of the cochlear portion of the vestibulocochlear nerve; hemorrhages in the vascular stria are not uncommon.

Quinine intoxication may be acute or chronic. Acute labyrinth intoxication occurs when large doses of quinine are used, exceeding the daily dose by two to three times (for adults - 1.2 g). The first symptom of acute quinine intoxication is a strong tinnitus, followed quickly by progressive hearing loss. These symptoms are accompanied by attacks of systemic dizziness caused by different damage to the right and left vestibular apparatus. After a few days, vestibular disorders and hearing loss gradually decrease; in some cases, an increase in the thresholds of auditory perception of tonal sounds at a frequency of 4000 Hz and adjacent frequencies remains.

Chronic intoxication occurs with prolonged use of quinine preparations. The main symptom is perceptual hearing loss, tinnitus is not pronounced, is periodic, and dizziness attacks rarely occur. Hearing loss is irreversible and tends to progress even after cessation of quinine.

Salicylates cause the same damage to the inner ear as quinine, but clinically less pronounced and, as a rule, reversible. Only as a result of long-term use of drugs of this group, permanent hearing loss may occur. Toxic doses, in addition to tinnitus, hearing loss and dizziness, cause excitement, euphoria, visual and respiratory disorders, delirium, soporosis, coma, nasal, gastrointestinal and uterine bleeding, peripheral edema. The development of methemoglobinemia is possible.

Treatment consists of forced diuresis and blood alkalization, hemodialysis and hemosorption. In case of bleeding caused by taking salicylates, vikasol, calcium chloride are prescribed; in case of excitation - aminazine; in case of methemoglobinemia - intravenous methylene blue in glucose solution, replacement blood transfusion.

Toxic labyrinthoses of professional etiology. Poisoning with industrial toxins is often accompanied by labyrinthoses of professional etiology. Professional poisoning is defined as pathological conditions caused by the effect on the human body (worker) of toxic substances that are an integral part of the technological process, and the poisoning itself is a consequence of non-compliance with safety precautions. Industrial toxins constitute a large group of toxic substances and compounds with various chemical and physical properties (gases, liquids, powders, aerosols, etc.), aggressive in nature and having a destructive effect on biological environments. In industrial conditions, toxic substances enter the body mainly by inhalation or in the form of industrial condensates through the gastrointestinal tract. They can also enter through the skin, into the gastrointestinal tract through contaminated hands, and with food products. Cochleovestibular lesions occur mainly in cases of intoxication with neurotropic poisons, which have a generalized effect on all parts of the nervous system, disrupting the processes of reception, conduction of nerve impulses and the functions of its central parts. In this case, peripheral cochleovestibular disorders are joined by disorders of a central nature.

Acute poisoning with neurotropic poisons is manifested by a combination of neurological, mental and somatovegetative symptoms, among which the most common are tinnitus and noise in the head, non-systemic dizziness, impaired coordination of movements, ataxia caused by dysfunction of the vestibular nuclei, vestibulospinal and vestibulocerebellar coordination. In addition, each individual type of intoxication has its own specific signs characteristic of the given poison, for example, damage to vision and excretory function of the kidneys in case of poisoning with methanol or damage to the kidneys and liver in case of poisoning with mercury compounds.

The most common form of industrial poisoning is chronic intoxication, which occurs during long-term work in conditions of non-observance of safety precautions and the action of relatively low concentrations of harmful substances. This is facilitated by the property of industrial poisons to accumulate in various organs and systems, forming potential depots from which, under the influence of certain unfavorable conditions, the accumulated poisons enter the blood and cause phenomena of general intoxication. Under these conditions, the most affected organs and systems are weakened by infection or other occupational hazards, for example, the receptors of the inner ear, exposed to professional noise or vibration. A feature of industrial poisoning is their group ("workshop") nature, the similarity of symptoms of the disease in large groups of people engaged in the same type of technological process.

Among industrial poisons capable of causing labyrinthosis of professional etiology, it is necessary to note such as acrolein, acetone, borohydrides, vinyl chloride, dioxane, isocyanates, salts of heavy metals, mercaptans, lead compounds (tetraethyl lead) and mercury, ethylene glycol and many others. The clinical manifestations of poisoning with which, the diagnosis of these poisonings and therapeutic measures are described in textbooks and manuals on toxicology. It should only be emphasized that along with the specific clinical signs characteristic of poisoning with each individual poison, there is also a "non-specific" sign - dizziness, the genesis of which is not clear enough, since the points of application of industrial poisons can be different - from the receptors of the vestibule to the vestibular nuclei and accumulations of gray matter of the cerebellum, including the cortical zones of the vestibular analyzer.

Diagnosis of toxic labyrinthosis is based on the anamnesis, access to the toxic substance, and specific signs of poisoning.

Treatment is carried out in specialized resuscitation and therapeutic departments or toxicology centers by removing the poison from the body, using specific antidotes and general symptomatic treatment.

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