Chronic acoustic trauma: causes, symptoms, diagnosis, treatment

Causes of chronic acoustic trauma. The cause of chronic acoustic trauma is intensive noise that lasts throughout the working time - an integral factor of the technological process in such industries as metallurgy and heavy engineering, textile industry, shipbuilding, labor activity with vibration equipment, engine building, aviation, etc. Chronic acoustic trauma is the cause of professional deafness.

Pathogenesis of chronic acoustic trauma. In the pathogenesis of occupational deafness, several hypotheses (theories) are considered: mechanical, adaptation-trophic, neurogenic, vascular and some other less significant. The mechanical theory explains the destructive changes in CnO that arise under the influence of noise by the physical destruction of the extremely fragile structures of this organ. As studies have shown, such a mechanism is possible with extremely intense low-frequency sound, but the theory does not explain the occurrence of structural changes in CsO and hearing loss with prolonged action of relatively weak sounds that are not capable of causing mechanical damage to CnO. Adaptation-trophic theory ascribes the main role to the phenomena of fatigue, exhaustion and degeneration of the structures of CnO that arise under the influence of metabolic disturbance in the VU and local disturbance of adaptation-trophic processes. Neurogenic theory explains the changes in CnD as a secondary phenomenon that occurs under the influence of primary pathological foci of excitation in the auditory and autonomic subcortical centers. The vascular theory attaches great importance to secondary metabolic disorders in the inner ear that arise under the influence of acoustic stress, the consequence of which are generalized dysfunctions in the body, called noise disease.

Pathogenesis is determined by two main factors: the characteristics of noise (frequency spectrum and intensity) and the susceptibility or property of the reverse - the individual resistance of the hearing organ to the damaging effect of noise.

Professionally harmful noise is one whose intensity exceeds the threshold of damage 90-100 dB; So, until recently, that is, in the second half of the 20th century, in textile industries, the noise intensity was 110-115 dB, and in the test bench - 135-145 dB. With a high sensitivity of the hearing organ to noise, loss of auditory sensitivity can occur with a prolonged action of the latter with an intensity of 50-60 dB.

The frequency spectrum of noise also plays an important role in the development of occupational deafness, with the most damaging effect being exerted by its high-frequency components. Low frequencies do not have a significant damaging effect on the CpO receptor apparatus, but at a considerable intensity, especially in the part of the spectrum approaching infrasound, the infrasound itself can have a mechanical destructive effect on the structures of the middle and inner ear (eardrum, aural ossicles, membranous formation of the cochlear lobule of the vestibular apparatus). It should be noted that the masking effect of low sounds with respect to high sounds, consisting in the "absorption" of the latter by a wave traveling along the basilar membrane, plays a peculiar protective mechanical and physiological role with respect to the CpO receptors, balancing the processes of their activation and inhibition.

Exposure of noise exposure determines the "accumulation" of the damaging effect of noise and is in fact the factor of probation of the individual in this production. In the process of exposing the noise effect, the hearing organ undergoes three stages of development of professional hearing loss:

1. the adaptation stage, at which there is a slight decrease in auditory sensitivity (by 10-15 dB); the termination of noise at this stage leads to the restoration of hearing to the normal (initial) level within 10-15 minutes;
2. with a longer exposure to noise, the stage of fatigue occurs (hearing loss by 20-30 dB, the occurrence of high-frequency subjective ear noise, hearing restoration occurs after several hours of stay in a quiet environment); At this stage, on the tonal audiogram, the so-called Karhart's tooth first appears;
3. the stage of organic changes in CnO, at which the loss of hearing becomes significant and irreversible.

Among other factors affecting the development of occupational deafness, it is necessary to note the following:

1. from two noises of equal intensity and frequency spectrum, intermittent noise has a more detrimental effect and less damaging effect is a constantly acting noise;
2. closed rooms with well-resounding walls and ceilings, dense in structure and therefore reflecting well (and not absorbing), poor ventilation, gas contamination and dustiness of the room, etc., as well as a combination of noise and vibration exacerbate the effect of noise on the hearing organ;
3. age; The most damaging effect of noise is experienced by persons over 40 years old;
4. presence of diseases of the upper respiratory tract, auditory tube and middle ear strengthens and accelerates the development of professional hearing loss;
5. organization of the labor process (application of means of individual and general protection, conducting preventive rehabilitation measures, etc.).

Pathological anatomy. Experiments on animals have shown that noise has a destructive effect on the structures of CnO. The first suffer from external hair cells and external phalangeal cells, then internal hair cells are involved in the degenerative process. Prolonged and intensive irradiation of animals with sound leads to total death of SpO, ganglion cells of the nerve spiral node and nerve fibers. The defeat of the hair cells of CpO begins in the first cochlear curl in the zone of perceived sound frequency of 4000 Hz. GG Kobrak (1963) explains this phenomenon by the fact that the damage to hair cells of CpO in the first cochlea of a cochlea due to the action of intense noise arises because the physiological sound conduction by means of auditory ossicles is replaced by a direct air impact of sound on the round window membrane located in the immediate proximity to the region of the basilar maximum reacting frequency of 4000 Hz.

Symptoms of occupational deafness consist of specific and nonspecific symptoms.

Specific symptoms relate to the auditory function, the disorders of which progress according to the length of service and have a typical perceptual character. Patients complain of subjective high-frequency ear noise, a decrease in hearing at the beginning of the disease to high sounds, then deafness is added to the middle and low frequencies, speech intelligibility and noise immunity worsen. Nonspecific symptoms are characterized by general fatigue, increased stress in solving production problems, drowsiness during working hours and sleep disturbance at night, decreased appetite, increased irritability, increasing signs of vegetovascular dystonia. The evolution of the disease undergoes four stages.

1. The initial period, or period of primary symptoms, occurs from the first days of being in a noisy environment (ear noise, light pain in the ears, and by the end of the working day - intellectual and physical fatigue). Gradually, after a few weeks, the hearing organ adapts to noise, but there is an increase in the sensitivity threshold to the sound of 4000 Hz with hearing loss at this frequency up to 30-35 dB, sometimes even more (the so-called Carhart tooth, which can occur even after one day of work in conditions of intensive production noise). After a few hours of rest, the threshold of sound perception returns to normal. Over time, irreversible changes occur in the corresponding hair cells and the Karhart tooth, reaching a level of 40 dB in terms of loss of auditory sensitivity, becomes permanent. As the research of V.Mitrofanov (2002) showed, the earliest (prenosological) sign of occupational deafness, when there are no distinct changes in the standard threshold audiogram, is an increase in the thresholds for frequencies of 16, 18 and 20 kHz, that is, when hearing in extended frequency range. This period, depending on the individual sensitivity of the worker and on the characteristics of production noise can last from several months to 5 years.
2. The period of the first clinical pause is characterized by some stabilization of the pathological process, while changes in the auditory function that have arisen in the previous period remain practically unchanged, pain and signs of fatigue pass, the general condition improves. This "light" gap, probably, arises under the influence of mobilization of adaptive and adaptive processes that play a protective role for a certain time. However, the "accumulation" of the damaging effect of noise continues, which is reflected in a tonal audiogram that gradually acquires a V-shape due to hearing loss at frequencies adjacent to the right and left to the tone of 4000 Hz tones covering 1-1 1/2 octaves. The perception of speaking in the absence of production noise does not suffer, whisper speech is perceived at a distance of 3-3.5 m. This period can last from 3 to 8 years.
3. The period of growth of clinical signs is characterized by progressive hearing impairment, constant ear noise, broadening of the frequency range with an increased sensitivity threshold towards both low (up to 2000 Hz) and high (8000 Hz) tones. The perception of spoken speech is reduced to 7-10 m, whispered - up to 2-2.5 m. In this period, the nonspecific symptoms of the "noise" disease are further developed. In this period, the achieved level of deafness can be maintained without further changes for the worse, even if the noise effect continues. In this case, talk about the period of the second clinical pause. This period can last from 5 to 12 years.
4. The terminal period occurs after 15-20 years of operation in conditions of industrial noise in persons with increased sensitivity to it. By this time, clear nonspecific signs of "noise sickness" develop, some people have internal diseases, as regards hearing, its deterioration is progressing. Whispered speech is either not perceived, or perceived by the shell, spoken language is at a distance of 0.5-1.5 m, loud speech is 3-5 m away. Speech intelligibility and noise immunity of the hearing organ sharply worsen. Significantly increases the threshold of perception of pure tones as due to a sharp decrease in sensitivity to tones above 4000 Hz, and by reducing the sensitivity to the low-frequency part of the spectrum of audible frequencies. At high frequencies of the tone threshold audiogram, breaks ("hatches") are formed. Progression of hearing loss in this period can attain hearing loss of up to 90-1000 dB. Ear noise becomes unbearable, often there are vestibular disorders in the form of dizziness and quantitative changes in the parameters of provocative nystagmus.

Evolution of professional hearing loss depends on many factors: from prevention and treatment tools, noise parameters, length of service, and also on the individual tolerability of the noise factor. In some cases, under favorable circumstances, the progression of hearing loss may stop at any of these periods, but for the most part, with continued noise effects, the hearing loss progresses to grade III and IV.

The treatment of occupational deafness is complex, multifaceted, including the use of medications, individual and collective prevention, as well as carrying out measures for the rehabilitation of hearing impairments. Treatment and other measures to prevent the development of occupational deafness are most effective if they are carried out in the first and second periods of the disease, and in the first period the effectiveness of prophylaxis of occupational deafness increases, and in the second period the backward development of hearing loss may occur, provided that noise is eliminated from working conditions. In the third period, only the suspension of further deterioration of hearing is possible, in the fourth period the effectiveness of treatment is completely absent.

Drug treatment for patients with professional hearing loss includes the use of drugs nootropic series (piracetam, nootropil), compounds of y-aminobutyric acid (aminalon, gamma-lon, GABA) in combination with ATP, B vitamins, microcirculation improvers (benzyclan, vencyclane , trental, cavinton, xanthinal nicotinate), antihypoxants (Aevit, complexes of vitamins and microelements). Medicamental treatment is advisable to be carried out simultaneously with HBO. Rehabilitation activities include sanatorium treatment, the provision of preventive courses of drug treatment in dispensaries. Important are the means of collective (engineering) and individual (the use of protective earmolds such as "ear plugs") prevention, exclusion of tobacco smoking, alcohol abuse.

[1], [2], [3], [4], [5], [6]