Hearing damage caused by noise can be divided into various subgroups:
Depending upon the intensity and duration of the damaging acoustic waves one differentiates between acoustic trauma, blast trauma, explosion trauma and acute noise trauma.
The sound pressure results in the loss of cells at the interface between the acoustic mechanical vibrations and the nerve signals in the cochlea in the inner ear (the corti organ), to damage to the outer hair cells, the support cells and also damage to many other anatomic structures . If one measures the partial oxygen pressure in the lymphs between the skin and the bony labyrinth of the inner ear (perilymph), one can measure a significant drop in pressure . Lack of oxygen in the cochlea prevents the functional metabolism of the cells, such that there is a loss of hearing.
By increasing the partial oxygen pressure in the cochlea, in particular in the area of the peri and endo lymphs, it is possible to influence hearing cells with a metabolic disorder. However, since these cells have no vessels supplying blood but only receive oxygen by way of diffusion, an oxygen deficiency situation can only be compensated in principle by raising the ambient oxygen partial pressure.
Moreover, hyperbaric oxygen therapy can, in the case of acute noise trauma, have a positive effect on the formation of oedema in the damaged inner ear. The clinical relevance of these processes is verified in a number of treatment studies [3-13].
An important point to note is that an acute loss of hearing caused by noise trauma remedies itself spontaneously in around half of all cases. These spontaneous remissions usually take place within the first 48 hours after the impact of the noise. If after that time there has been no significant improvement in the symptoms, hyperbaric oxygen therapy is indicated, since after that time spontaneous remission only takes place very rarely.
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