Definition and Causes

Sensorineural hearing loss, or nerve-related deafness, is a sudden or rapidly progressive loss of hearing related to problems with the inner ear and the nerves that connect the ear to the brain.

Sudden hearing loss is commonly defined as a reduction in sound volume greater than 30 dB (decibels) across three connected frequencies in a 72-hour period.

Doctors and patients cannot usually pinpoint a specific cause for sensorineural hearing loss. Researchers have confirmed a strong association with circulatory problems or lack of oxygen in the inner ear. Other possible causes include heredity, viral and bacterial infection, toxins, growths or tumors, poor nutrition, injury or trauma, nervous system disorders, and exposure to loud noise.

As many as 20 per 100,000 people per year experience sensorineural hearing loss. Nearly all cases (9 in 10) involve only one ear. Hearing loss is often accompanied by dizziness or ringing in the ear (tinnitus).

Many recover without treatment, but swift medical attention increases the chances for partial or full restoration of hearing.

Treatment with Hyperbaric Oxygen Therapy

Hyperbaric oxygen therapy (HBOT) is indicated for the treatment of idiopathic sudden sensorineural hearing loss.

Idiopathic means the exact cause is unknown. Sudden means the loss develops all at once or over a few days.

HBOT increases oxygen tension in the blood and tissues and dissolves extra oxygen in the blood plasma to better supply the structures, fluids, and nerves of the inner ear.

Physicians may prescribe HBOT in conjunction with corticosteroids to reduce inflammation and swelling.


Undersea and Hyperbaric Medical Society

Mechanisms of HBO2

The rationale for the use of hyperbaric oxygen to treat ISSHL is supported by an understanding of the high metabolism and paucity of vascularity to the cochlea. The cochlea and the structures within it require a high oxygen supply. The direct vascular supply, particularly to the organ of Corti, is minimal. Tissue oxygenation to the structures within the cochlea occurs via oxygen diffusion from cochlear capillary networks into the perilymph and the cortilymph. The perilymph is the primary oxygen source for these intracochlear structures. Unfortunately, perilymph oxygen tension is decreased significantly in patients with ISSHL. To achieve a consistent rise of perilymph oxygen content, the arterial-perilymphatic oxygen concentration difference must be extremely high. This can be restored with hyperbaric oxygen therapy.

Patients with moderate to profound ISSHL (= 41 dB) who present within 14 days of symptom onset should be considered for HBO2. While patients presenting after this time may experience improvement when treated with HBO2, the medical literature suggests that early intervention is associated with improved outcomes. The best evidence supports the use of HBO2 within two weeks of symptom onset.

Clinical management

Patients who present with ISSHL should undergo a complete evaluation by an otolaryngologist and audiologist, inclusive of appropriate audiological and imaging studies, to determine the degree and potential etiology of disease. Patients determined to have ISSHL and meet the selection criteria may benefit from HBO2.

The recommended treatment profile consists of 100% O2 at 2.0 to 2.5 atmospheres absolute for 90 minutes daily for 10 to 20 treatments.

Patients with no known contraindications to steroid therapy should also be treated concomitantly with oral corticosteroids.

Continued consultation and follow-up with an otolaryngologist is recommended.

 

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