No preferred treatment regimen exists for sudden hearing loss.
Treatment can be based upon a rational approach. Based on the history, physical examination findings, and laboratory results, if no definitive or treatable etiology is found, the treatment regimen should be dictated by the most likely factors involved. Remembering that all the medications used in treatment of sudden sensory hearing loss have potential adverse effects, the best course of action must be agreed upon by the physician and the patient.
The treatment regimens for ISSHL are varied, and this diversity reflects both the different etiologies that may cause sudden hearing loss and the uncertainty in diagnosis. The therapies can be grouped by mechanism of action. Experimental outcomes for some of these therapies are discussed under Prognosis.
Theoretically, vasodilators improve the blood supply to the cochlea, reversing hypoxia. In general, these are agents with effects on the systemic vasculature. Papaverine, histamine, nicotinic acid, procaine, niacin, and carbogen (5% carbon dioxide) have been used in attempts to improve cochlear blood flow. Carbogen inhalation has been shown to increase perilymph oxygen tension. Carbogen has also increased measured transcutaneous and subcutaneous oxygen tension without significantly affecting carbon dioxide tension. A study found that the efficiency of carbogen combined with drugs is superior to drug therapeutics in the treatment of sudden deafness. 
By altering blood viscosity with the use of low molecular weight dextrans, pentoxifylline, or anticoagulants (eg, heparin, warfarin), better oxygen delivery might be achieved. Dextrans cause a hypervolemic hemodilution and affect factor VIII, with both these effects influencing blood flow. Pentoxifylline affects platelet deformability, presumably improving blood flow. Anticoagulants interfere with the coagulation cascade as a mechanism to avoid formation of thrombi and emboli.
Corticosteroids are the primary anti-inflammatory agents used to treat ISSHL. The mechanism of action in sudden hearing loss is unknown, although reduction of cochlear and auditory nerve inflammation is the presumed pathway. However, the value of steroids in the treatment of idiopathic sudden sensorineural hearing loss (ISSNHL) remains unclear. 
In a randomized controlled study, intratympanic injection of dexamethasone is shown to effectively improve hearing in patients with severe or profound SSNHL after treatment failure with standard therapy and is not associated with major side effects.  Similar results were reported in yet another recent study.  Its trial to salvage hearing in cases where other medical therapy fails is justified.
A prospective study by Battaglia et al indicated that a greater percentage of patients with ISSNHL recover following combination therapy with high-dose prednisone taper (HDPT) and intratympanic dexamethasone (IT-Dex) than do those treated with HDPT alone. The investigators found that among those individuals with class-D hearing, 49% of patients who underwent combination therapy (10 mg/mL of IT-Dex every week for 3 wks, administered concomitantly with 60 mg/day of HDPT for 7 days, with a 7-day taper) recovered a serviceable amount of hearing, compared with 29% of patients who received only HDPT. It was also found that the likelihood of hearing recovery was higher when combination therapy was administered within 7 days of the onset of ISSNHL, with 56% of class-D patients achieving serviceable hearing. 
A paucity of data exists on the use of nonsteroidal anti-inflammatory agents.
Acyclovir and amantadine have had limited use in treating ISSHL, presuming a viral etiology. Two newer agents, famciclovir and valacyclovir, have not yet been reported upon as treatment for sudden hearing loss. They are structurally similar to acyclovir, affecting viral thymidine kinase. They inhibit viral DNA polymerase, preventing viral DNA replication.
Under the assumption that some episodes of ISSHL are secondary to cochlear endolymphatic hydrops, diuretic therapy has been used as treatment. As in Ménière disease, the mechanism of action for diuretics in sudden hearing loss is not understood.
Triiodobenzoic acid derivatives
These agents are thought to affect the stria vascularis and assist in maintaining the endocochlear potential. Diatrizoate meglumine, an angiographic contrast agent, was rather serendipitously found to have an effect on sudden hearing loss and is the most commonly used derivative of triiodobenzoic acid.
Presumably by increasing oxygen tension, hyperbaric oxygen has been evaluated as therapy for sudden hearing loss. The reported series are small, but the topic has been reviewed by Lamm et al in 1998. 
A study by Narozny (2004) concluded that hyperbaric oxygen therapy (consisting of exposure to 100% oxygen at a pressure of 250 kPa for a total of 60 minutes) in a multi-place hyperbaric chamber with high doses of glucocorticoids improves the results of conventional sudden sensorineural hearing loss treatment; the best results are achieved if the treatment is started as early as possible. 
Some other authors also believe that for people with early presentation of idiopathic sudden sensorineural hearing loss, the application of hyperbaric oxygen therapy can significantly improve hearing loss. However, a beneficial effect of hyperbaric oxygen therapy on chronic presentation of idiopathic sensorineural hearing loss and/or tinnitus is not evident. 
Repair of oval and round window perilymph fistulae (PLF) has been used in cases of ISSHL associated with a positive fistula test result or a history of recent trauma or barotrauma.
Perilymph leaks could produce sudden hearing loss in accordance with the intracochlear membrane rupture theory. Alternatively, low perilymph pressure could produce a relative state of cochlear endolymphatic hydrops.
Controversy exists regarding the role of surgical repair of perilymphatic fistulae because no universal standard exists for positive identification of a fistula. The tau transferrin test on perilymph fluid has not proven to be useful in the diagnosis of this entity.
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