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Degenerative labyrinthotoxicosis: causes, symptoms, diagnosis, treatment

 
, medical expert
Last reviewed: 23.04.2024
 
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Neomycin selectively acts on the cochlear hair cells of the cochlear snail and more often causes more frequent and deeper hearing damage than streptomycin, down to total 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 the cells), in the outer hair cells of CpO, in the fibers of the cochlea of the pre-collateral nerve cochlear; Hemorrhages in the vascular stria are common.

Intoxication with quinine can be acute and chronic. Acute intoxication of the labyrinth occurs with the use of large doses of quinine, exceeding in two to three times the daily dose (for adults - 1.2 g). The first symptom of acute intoxication with quinine is a strong ear noise, followed by rapid onset of progressive hearing loss. These symptoms are accompanied by attacks of systemic dizziness caused by unequal lesion of the right and left vestibular apparatus. After a few days, vestibular disorders and hearing loss gradually decrease; in some cases, the thresholds of auditory perception of tonal sounds at a frequency of 4000 Hz and neighboring frequencies are preserved.

Chronic intoxication occurs with prolonged use of quinine drugs. The main symptom is perceptual hearing loss, ear noise is not expressed, is periodic in nature, seldom there are attacks of dizziness. Hearing loss is irreversible and tends to progress even after quinine is discontinued.

Salicylates cause the same damage to the inner ear as quinine, but they are less clinically expressed and, as a rule, reversible. Only as a result of long-term use of drugs of this group can there be a permanent deafness. Toxic doses, in addition to tinnitus, hearing loss and dizziness, cause excitement, euphoria, visual disturbance, respiration, nausea, co-morbidity, coma, nasal, gastrointestinal and uterine bleeding, peripheral edema. Possible development of methemoglobinemia.

Treatment consists in forced diuresis and blood alkalization, in the use of hemodialysis and hemosorption. When bleeding caused by the intake of salicylates, appoint Vikasol, calcium chloride; with excitation, aminazine; with methemoglobinemia - intravenously methylene blue in a glucose solution, a replacement blood transfusion.

Toxic labyrinthosis of professional etiology. Often poisoning with industrial poisons is accompanied by labyrinthines of professional etiology. Professional poisoning is defined as pathological conditions caused by exposure to the body of a person (worker) of toxic substances that are an integral part of the technological process, and poisoning itself as a result of non-observance of safety procedures. Industrial poisons constitute a large group of toxic substances and compounds with a variety of chemical and physical properties (gases, liquids, powders, aerosols, etc.) that are aggressive in nature and have a destructive effect on biological environments. Under production conditions, toxic substances enter the body mainly by inhalation or in the form of industrial condensates through the digestive tract. It is also possible for them to enter through the skin, in the gastrointestinal tract through contaminated hands, and also with food. Cochleovestibular lesions occur mainly during intoxication with neurotropic poisons, which have a generalized effect on all parts of the nervous system, disrupting the processes of reception, carrying out nerve impulses and the functions of its central divisions. In this case, violations of the central character are added to the peripheral cochleovestibular disorders.

Acute poisoning with poisons of neurotropic action is manifested by a combination of neurological, psychiatric and somatovegetative symptoms, among which the most frequent are tinnitus and head dysfunction, dyspnoea, impaired coordination of movements, ataxia due to impaired vestibular nucleus, vestibulospinal and vestibulocerebellar coordination. In addition, for each individual type of intoxication, specific characteristics are observed for a given poison, for example, damage to the eyes and excretory function of the kidneys during methanol poisoning or kidney and liver damage when mercury compounds are poisoned.

The most frequent form of industrial poisoning is chronic intoxication, arising during long-term work in the conditions of non-compliance with safety procedures and the action of relatively low concentrations of harmful substances. This is promoted by the property of industrial poisons to be cumulated in various organs and systems, forming potential depots, from which, under the influence of certain unfavorable conditions, accumulated poisons enter the bloodstream and cause common intoxication. Under these conditions, the organs and systems weakened by infection or other occupational diseases, such as the inner ear receptors exposed to professional noise or vibration, become the most affected. The peculiarity of industrial poisoning is their group ("shop") nature, the similarity of the symptoms of the disease in large groups of individuals engaged in the same type of technological process.

Among industrial poisons capable of causing labyrinthosis of professional etiology, mention should be made of acrolein, acetone, borohydrides, vinyl chloride, dioxane, isocyanates, heavy metal salts, mercaptans, lead compounds (tetraethyl lead) and mercury, ethylene glycol and many others. Etc., the clinical manifestations of poisoning which, the diagnosis of these poisonings and therapeutic measures are described in textbooks and guidelines on toxicology. It should only be emphasized that along with the specific clinical signs peculiar to poisoning by each individual poison, there is also a "nonspecific" sign - dizziness, the genesis of which is not clear enough, since the points of application of industrial poisons can be different - from the vestibular receptors to the vestibular nuclei and clusters of gray substances of the cerebellum, including the cortical zones of the vestibular analyzer.

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

Treatment is carried out in specialized resuscitative and therapeutic departments or toxicological centers by removing the poison from the body, the use of specific antidotes and general symptomatic treatment.

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