eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Inner Ear
Inner Ear, Sudden Hearing Loss: Treatment & Medication
Updated: Feb 6, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
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.
- Vasodilators: 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.8
- Rheologic agents: 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.
- Anti-inflammatory agents
- 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 remains unclear.9
- In a recent 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.10 Similar results were reported in yet another recent study.11 Its trial to salvage hearing in cases where other medical therapy fails is justified.
- A paucity of data exists on the use of nonsteroidal anti-inflammatory agents.
- Antiviral 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.
- Diuretics: 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.
- Hyperbaric oxygen: 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 1998.12
- 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.13
- 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.14
Surgical Care
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.
Medication
No high-quality, randomized, controlled trial exists demonstrating the efficacy of any medical therapy in ISSHL. Hence, no single treatment has been unequivocally shown to be effective, but many strategies have been proposed. Carbogen (5% CO2 +95% oxygen) inhaled for 30 min, 6 times per day (q2h during the day) for 5 days has been used.15
Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Prednisone (Orasone, Meticorten, Deltasone, Wysolone)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
Adult
60 mg PO qd for 10 d, then taper by 5 mg qd (the taper is not strictly necessary)
Pediatric
1 mg/kg PO qd for 10 d with taper if desired
Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
Dexamethasone (Decadron)
Intratympanic dexamethasone increases cochlear blood flow after ischemia-induced injury.
Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.
Adult
0.3–0.4 mL solution of dexamethasone (8 mg/mL) with hyaluronidase by intratympanic route on alternate days
Pediatric
Not established
Effects decrease with coadministration of barbiturates, phenytoin and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Diuretics
These agents are beneficial in the treatment of fluid retention.
Hydrochlorothiazide/triamterene (Dyazide, Maxzide)
Inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.
Adult
25 mg (hydrochlorothiazide)/50 mg (triamterene) PO qod
Pediatric
Not established
Thiazides may decrease effects of anticoagulants, antigout agents, and sulfonylureas; thiazides may increase toxicity of allopurinol, anesthetics, antineoplastics, calcium salts, loop diuretics, lithium, diazoxide, digitalis, amphotericin B, and nondepolarizing muscle relaxants
Documented hypersensitivity; anuria; renal decompensation
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal disease, hepatic disease, gout, diabetes mellitus, and erythematosus
Skin and mucus membrane agents
Agents in this category may help in the dispersion and absorption of drugs.
Hyaluronidase (Hylase, Wydase Injection)
Stimulates hydrolysis of hyaluronic acid, one of the chief ingredients of tissue cement, which offers resistance to diffusion of liquids through tissues. Used to aid in absorption and dispersion of injected drugs
Intratympanic hyaluronic acid may increase permeability of membranes and influences distribution of dexamethasone within inner ear.
Adult
Administer 0.2 mg/mL with dexamethasone by intratympanic route on alternate days (1-7 injections)
Pediatric
Not established
Salicylates, cortisone, ACTH, estrogens, and antihistamines may decrease effects of hyaluronidase
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Avoid injecting into inflamed or cancerous areas; perform intradermal skin test for sensitivity before initiating infusion; discontinue if sensitivity or extravasation occur
More on Inner Ear, Sudden Hearing Loss |
| Overview: Inner Ear, Sudden Hearing Loss |
| Differential Diagnoses & Workup: Inner Ear, Sudden Hearing Loss |
Treatment & Medication: Inner Ear, Sudden Hearing Loss |
| Follow-up: Inner Ear, Sudden Hearing Loss |
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References
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Further Reading
Keywords
hearing loss, sudden hearing loss, sudden deafness, sudden sensorineural hearing loss, idiopathic sudden sensory hearing loss, ISSHL, hearing problems, hearing
Treatment & Medication: Inner Ear, Sudden Hearing Loss