Chronic acoustic trauma: causes, symptoms, diagnosis, treatment

Causes of chronic acoustic trauma. The cause of chronic acoustic trauma is intense and long-term noise throughout the working hours - an integral factor of the technological process in such industries as metallurgy and heavy engineering, textile industry, shipbuilding, work with vibration installations, motor engineering, aviation, etc. Chronic acoustic trauma is the cause of occupational hearing loss.

Pathogenesis of chronic acoustic trauma. Several hypotheses (theories) are considered in the pathogenesis of occupational hearing loss: mechanical, adaptive-trophic, neurogenic, vascular and some others, less significant. The mechanical theory explains the destructive changes in the SpO that occur 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 sounds of the low-frequency spectrum, but the theory does not explain the occurrence of structural changes in the SpO and hearing loss with long-term exposure to relatively weak sounds that are not capable of causing mechanical damage to the SpO. The adaptive-trophic theory attributes the main role to the phenomena of fatigue, exhaustion and degeneration of the SpO structures that occur under the influence of metabolic disorders in the external auditory canal and local disruption of adaptive-trophic processes. The neurogenic theory explains changes in SpO as a secondary phenomenon arising under the influence of primary pathological excitation foci in the auditory and vegetative subcortical centers. The vascular theory attaches great importance to secondary metabolic disorders in the inner ear arising under the influence of acoustic stress, the consequence of which is generalized dysfunction in the body, called noise disease.

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

Occupationally harmful noises are those whose intensity exceeds the damage threshold of 90-100 dB; thus, until recently, i.e. in the second half of the 20th century, in textile production the noise intensity was 110-115 dB, and at jet turbine test stands - 135-145 dB. With high sensitivity of the hearing organ to noise, loss of hearing sensitivity can occur with prolonged exposure to the latter with an intensity of 50-60 dB.

The frequency spectrum of noise also plays an important role in the development of occupational hearing loss, with its high-frequency components having the most damaging effect. Low frequencies do not have a pronounced damaging effect on the receptor apparatus of the SpO, but at significant intensity, especially in the part of the spectrum approaching infrasound, and infrasound itself, can have a mechanical destructive effect on the structures of the middle and inner ear (eardrum, chain of auditory ossicles, membranous formations of the cochlea of the vestibular apparatus). It should be noted that the masking effect of low sounds in relation to high ones, consisting in the "absorption" of the latter by a wave running along the basilar membrane, plays a kind of protective mechanical and physiological role in relation to the receptors of the SpO, balancing the processes of their activation and suppression.

Exposure to noise determines the "accumulation" of the damaging effect of noise exposure and is actually a factor in the length of service of a given individual in a given production. During exposure to noise, the hearing organ undergoes three stages of development of occupational hearing loss:

1. adaptation stage, during which there is some decrease in hearing sensitivity (by 10-15 dB); cessation of noise at this stage leads to restoration of hearing to a normal (initial) level within 10-15 minutes;
2. with longer exposure to noise, a stage of fatigue occurs (hearing loss of 20-30 dB, the appearance of high-frequency subjective tinnitus; hearing recovery occurs after several hours in a quiet environment); at this stage, the so-called Carhart wave first appears on the tonal audiogram;
3. the stage of organic changes in the SpO, at which hearing loss becomes significant and irreversible.

Among other factors influencing the development of occupational hearing loss, the following should be noted:

1. of two noises that are identical in intensity and frequency spectrum, intermittent noise has a more harmful effect and continuous noise has a less damaging effect;
2. the confined spaces of rooms with well-resonating walls and ceilings, dense in structure and therefore well reflecting (and not absorbing) sounds, poor ventilation, gas and dust pollution of the room, etc., as well as the combination of noise and vibration aggravate the effect of noise on the organ of hearing;
3. age; the most damaging effects of noise are experienced by people over 40 years of age;
4. the presence of diseases of the upper respiratory tract, auditory tube and middle ear intensifies and accelerates the development of occupational hearing loss;
5. organization of the work process (use of personal and general protective equipment; implementation of preventive rehabilitation measures, etc.).

Pathological anatomy. Animal experiments have shown that noise has a destructive effect on the structures of the SpO. The outer hair cells and outer phalangeal cells are the first to suffer, then the inner hair cells are involved in the degenerative process. Long-term and intense irradiation of animals with sound leads to total death of the SpO, ganglion cells of the nervous spiral ganglion and nerve fibers. Damage to the hair cells of the SpO begins in the first curl of the cochlea in the zone of the perceived sound frequency of 4000 Hz. G.G. Kobrak (1963) explains this phenomenon by the fact that damage to the hair cells of the SpO in the first curl of the cochlea under the influence of intense noise occurs due to the fact that physiological sound conduction through the auditory ossicles is replaced by the direct air effect of sound on the membrane of the round window, located in close proximity to the basilar zone with a maximum response frequency of 4000 Hz.

Symptoms of occupational hearing loss consist of specific and non-specific symptoms.

Specific symptoms concern the auditory function, the impairment of which progresses depending on the length of service and has a typical perceptual character. Patients complain of subjective high-frequency tinnitus, hearing loss at the beginning of the disease for high sounds, then hearing loss for medium and low frequencies, deterioration of speech intelligibility and noise immunity. Non-specific symptoms are characterized by general fatigue, increased stress when solving production problems, drowsiness during working hours and sleep disturbance at night, decreased appetite, increased irritability, increasing signs of vegetative-vascular dystonia. The evolution of the disease undergoes four stages.

1. The initial period, or the period of primary symptoms, occurs from the first days of exposure to a noisy environment (tinnitus, mild pain in the ears, and by the end of the working day - intellectual and physical fatigue). Gradually, after several weeks, the hearing organ adapts to the noise, but there is an increase in the threshold of sensitivity to sound of 4000 Hz with hearing loss at this frequency of up to 30-35 dB, sometimes more (the so-called Carhart's tooth, which can occur even after one day of work in conditions of intense industrial noise). After several hours of rest, the threshold of sound perception returns to normal. Over time, irreversible changes occur in the corresponding hair cells and the Carhart's tooth, reaching a level of 40 dB in terms of hearing loss, becomes permanent. As shown by the research of V.V. Mitrofanov (2002), the earliest (pre-clinical) sign of occupational hearing loss, when there are no clear changes in the standard threshold audiogram, is an increase in thresholds at frequencies of 16, 18 and 20 kHz, i.e., when examining hearing in an extended frequency range. This period, depending on the individual sensitivity of the worker and the characteristics of industrial 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 the changes in the auditory function that arose in the previous period remain virtually unchanged, pain and signs of fatigue pass, and the general condition improves. This "bright" interval probably occurs under the influence of the mobilization of adaptive and adjustment processes that play a protective role for a certain time. However, the "accumulation" of the damaging effect of noise continues, which is reflected in the tonal audiogram, gradually acquiring a V-shaped appearance due to hearing loss at frequencies adjacent to the right and left of the 4000 Hz tone, tones covering 1-1 1/2 octaves. Perception of spoken language in the absence of industrial noise does not suffer, whispered speech is perceived at a distance of 3-3.5 m. This period can last from 3 to 8 years.
3. The period of increasing clinical signs is characterized by progressive hearing impairment, constant tinnitus, expansion 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 language decreases to 7-10 m, whispered speech - to 2-2.5 m. During this period, non-specific symptoms of "noise" disease develop further. During this period, the achieved level of hearing loss can be maintained without further changes for the worse, even if noise exposure continues. In this case, they talk about the period of the second clinical pause. This period can last from 5 to 12 years.
4. The terminal period begins after 15-20 years of work in conditions of industrial noise in individuals with increased sensitivity to it. By this time, distinct non-specific signs of "noise disease" develop, a number of individuals develop diseases of the internal organs, as for hearing, its deterioration progresses. Whispered speech is either not perceived or is perceived at the auricle, conversational speech - at a distance of 0.5-1.5 m, loud speech - at a distance of 3-5 m. Speech intelligibility and noise immunity of the hearing organ deteriorate sharply. The threshold of perception of pure tones increases significantly both due to a sharp decrease in sensitivity to tones above 4000 Hz, and due to a decrease in sensitivity to the low-frequency part of the spectrum of audible frequencies. Breaks ("hatches") are formed at high frequencies of the tonal threshold audiogram. The progression of hearing loss in this period can reach a hearing loss of up to 90-1000 dB. The tinnitus becomes unbearable, and vestibular disorders often appear in the form of dizziness and quantitative changes in the parameters of provocative nystagmus.

The evolution of occupational hearing loss depends on many factors: prevention and treatment methods, noise parameters, length of service, and individual tolerance to the noise factor. In some cases, under favorable circumstances, the progression of hearing loss may stop in any of the above periods, but in most cases, with continued exposure to noise, hearing loss progresses to grades III and IV.

Treatment of occupational hearing loss is complex, multifaceted, including the use of medication, individual and collective prevention, as well as measures to rehabilitate hearing loss. Treatment and other measures to prevent the development of occupational hearing loss are most effective if they are carried out in the first and second periods of the disease, with the effectiveness of prevention of occupational hearing loss increasing in the first period, and reverse development of hearing loss possible in the second period, provided that noise is excluded from working conditions. In the third period, only a halt in further hearing deterioration is possible, while in the fourth period, treatment is completely ineffective.

Drug treatment of patients suffering from occupational hearing loss includes the use of nootropic drugs (piracetam, nootropil), compounds of y-aminobutyric acid (aminalon, gammalon, GABA) in combination with ATP, B vitamins, drugs that improve microcirculation (bencyclane, vencyclane, trental, cavinton, xanthinol nicotinate), antihypoxants (aevit, vitamin and microelement complexes). Drug treatment should be carried out simultaneously with HBO. Rehabilitation measures include spa treatment, preventive courses of drug treatment in health centers. Important are the means of collective (engineering) and individual (use of protective ear plugs) prevention, elimination of smoking, alcohol abuse.

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