AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Background

Definitions of sudden hearing loss have been based on severity, time course, audiometric criteria, and frequency spectrum of the loss. Abrupt as well as rapidly progressive losses have been included under a single definition of sudden hearing loss. Awakening with a hearing loss, hearing loss noted over a few days, selective low- or high-frequency loss, and distortions in speech perception have all been classified as sudden hearing losses. A commonly used criterion to qualify for this diagnosis is a sensorineural hearing loss of greater than 30 dB over 3 contiguous pure-tone frequencies. Fortunately, the vast majority of cases of sudden hearing loss are unilateral, and the prognosis for some recovery of hearing is good. Usually it presents as unilateral loss of hearing; bilateral involvement is rare, and simultaneous bilateral involvement is very rare.

Sudden deafness or sudden SNHL and has many possible etiologies.

Pathophysiology

The postulated pathophysiology for idiopathic sudden sensory hearing loss (ISSHL) has 4 theoretical pathways. These are labyrinthine viral infection, labyrinthine vascular compromise, intracochlear membrane ruptures, and immune-mediated inner ear disease. A disease process involving any of these theoretical possibilities could have sudden hearing loss as a symptom. Each theory may explain a fraction of the episodes of sudden sensory hearing loss, but none of the existing theories individually could account for all episodes.

Viral infection

The evidence to implicate viral infection as one cause of sudden idiopathic sensory hearing loss is circumstantial. Studies of patients with ISSHL show a moderate prevalence of recent viral-type illness. Sometimes, evidence of recent viral seroconversion or inner ear histopathology consistent with viral infection is present.

The weakest of these links is the history of a recent viral illness. Noncontrolled studies report that 17-33% of patients recall a recent viral illness. Should those numbers seem significant, 25% of patients without hearing loss visiting an otolaryngology clinic had experienced a viral-like illness within a month.

Comparing patients experiencing ISSHL with control patients has produced some evidence of viral seroconversion. Rates of seroconversion for the herpesvirus family were significantly higher in the population of patients with sudden hearing loss.

Finally, temporal bone histopathologic studies of patients who experienced ISSHL found damage in the cochlea consistent with viral injuries. Loss of hair cells and supporting cells, atrophy of the tectorial membrane, atrophy of the stria vascularis, and neuronal loss were observed. These patterns were similar to findings in documented cases of hearing loss secondary to mumps, measles, and maternal rubella. Viral infection can be implicated as a cause of ISSHL, but this cannot, as yet, be proven. Infections with mumps virus provide the best model for a virally induced sensorineural hearing loss. In one study of ISSHL, subclinical mumps infections were documented in 9 of 130 patients by positive immunoglobulin M (IgM) mumps antibodies.

Vascular compromise

The cochlea is an end organ with respect to its blood supply, with no collateral vasculature. Cochlear function is exquisitely sensitive to changes in blood supply. Vascular compromise of the cochlea due to thrombosis, embolus, reduced blood flow, or vasospasm seems to be a likely etiology for ISSHL. The time course correlates well with a vascular event, a sudden or abrupt loss. A reduction in oxygenation of the cochlea is the likely consequence of alterations in cochlear blood flow. Alterations in perilymph oxygen tension have been measured in response to changes in systemic blood pressure or intravascular carbon dioxide partial pressure (pCO₂).

Histologic evidence of cochlear damage following occlusion of the labyrinthine vessels was documented in temporal bone studies in animals and humans. Intracochlear hemorrhage was noted as an early development; subsequently, fibrosis and ossification of the cochlea evolved.

In a study, a partial overlap was found between classical coronary risk factors and risk factors for sudden hearing loss. Hypercholesterolemia and hypoalphalipoproteinemia (low HDL cholesterol levels) were not found to be apparent major risk factors for sudden hearing loss, whereas the GPIa C807T polymorphism, elevated fibrinogen levels, and smoking were associated with an increased risk for ISSHL. Altogether these findings suggested a vascular involvement in the pathogenesis of ISSHL. This may have important implications for the development of therapeutic and preventive strategies for ISSHL (Rudack et al, 2006).

Intracochlear membrane rupture

Thin membranes separate the inner ear from the middle ear, and within the cochlea, delicate membranes separate the perilymphatic and endolymphatic spaces. Rupture of either or both sets of membranes theoretically could produce a sensory hearing loss. A leak of perilymph fluid into the middle ear via the round window or oval window has been postulated to produce hearing loss by creating a state of relative endolymphatic hydrops or by producing intracochlear membrane breaks. Rupture of intracochlear membranes would allow mixing of perilymph and endolymph, effectively altering the endocochlear potential. The theory of intracochlear membrane rupture was favored by Simmons and Goodhill, and histologic evidence has been documented by Gussen (Simmons, 1968; Goodhill, 1979; Gussen, 1981).

Immune-mediated inner ear disease

Sensorineural hearing loss induced by an immune process has gained greater and greater notoriety since the concept was introduced in 1979. Progressive sensorineural loss is observed with this condition. Whether or not sudden hearing loss occurs with immune-mediated inner ear disease is unclear, but immunologic activity in the cochlea is supported by greater and greater evidence. The association of hearing loss in Cogan syndrome, systemic lupus erythematosus, and other autoimmune rheumatologic disorders has been well documented. With better markers for inner ear autoimmunity, perhaps a greater linkage with ISSNHL will be found. A recent prospective study on 51 patients with ISSNHL supported the existence of multiple immune-mediated disorders in these patients (Toubi et al, 2004).

Frequency

United States

Estimates of the annual incidence of sudden sensory hearing loss range from 5-20 cases per 100,000 persons. Many cases likely go unreported, and the incidence may be higher. A sudden hearing loss may resolve before the patient can be evaluated medically, making it unlikely for that individual to seek care.

Sex

Female-to-male distribution appears to be equal. Combined data from several studies show a slight male preponderance, at 53%. However, a single large study of 1220 patients had slightly more females. Sex does not seem to be a risk factor. An equal distribution of right- and left-sided cases should be expected. As with sex, no greater risk for right-sided losses compared to left-sided losses seems to exist. Bilateral sudden hearing loss occurs in approximately 1-2% of cases.

Age

People of all age groups are affected by sudden hearing loss, but fewer cases are reported in children and the elderly. The peak incidence appears to be in the sixth decade of life. Young adults have incidence rates similar to those of middle-aged adults. The median age at presentation ranges from 40-54 years. The occurrence of sudden hearing loss across all age groups is an indication of the multifactorial nature of this clinical problem.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

Sudden sensorineural hearing loss has been called an otologic emergency. Patient evaluation should proceed promptly and expeditiously. Early presentation to a physician and early institution of treatment improves the prognosis for hearing recovery. The immediate goal is discovering a treatable or defined cause of the sudden hearing loss.

• Information about the onset, time course, associated symptoms, and recent activities may be helpful.
• Past medical history may reveal risk factors for hearing loss.
• • All medications, including over-the-counter products, must be described.
  • Aspirin can cause a reversible sensorineural hearing loss, and the list of aspirin-containing products is extensive.

Physical

Perform a careful head and neck examination, with special attention to the otologic and neurologic examination.

Tuning fork tests and fistula test using pneumatic speculum must be performed.

Causes

• The term sudden hearing loss encompasses defined causes and ISSHL. In the evaluation of a sudden sensorineural hearing loss, a definite etiology may be uncovered. The following have been associated with sudden hearing loss:
• • Infection - Bacterial (eg, meningitis, syphilis), viral (eg, mumps, cytomegalovirus, varicella/zoster)
  • Inflammation - Sarcoidosis, Wegener granulomatosis, Cogan syndrome
  • Vascular - Hypercoagulable states (eg, Waldenstrom macroglobulinemia), emboli (eg, post–coronary artery bypass graft [CABG] surgery), post–radiation therapy
  • Tumor - Vestibular schwannoma, temporal bone metastases, carcinomatous meningitis
  • Trauma - Temporal bone fracture, acoustic trauma, penetrating temporal bone injuries
  • Toxins - Aminoglycoside antimicrobials, cisplatin
• The greater number of cases, however, fits into the idiopathic category. ISSHL is the frustrating endpoint for most patients with sudden hearing loss.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Infection/Inflammation of cochlea/auditory nerve

Viral infection of cochlea/auditory nerve
Syphilis
Meningitis
Encephalitis

Neoplasms

Acoustic neuroma (vestibular schwannoma)
Other cerebellopontine angle (CPA) tumors

Vascular abnormalities

Sludging due to hyperviscosity
Polycythemia vera
Macroglobulinemia
Leukemia
Accelerated coagulation
Arteriosclerosis
Aneurysm of anterior inferior cerebellar artery

Endocrine abnormalities

Hypothyroidism
Diabetes mellitus

Multiple sclerosis

Congenital anomalies

Mondini dysplasia
Enlarged vestibular aqueduct

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• Laboratory studies should be directed by the history and physical examination findings.
• • Fluorescent treponemal antibody-absorption (FTA-Abs) for syphilis
  • Antinuclear antibodies (ANA), rheumatoid factor, and erythrocyte sedimentation rate (ESR) for autoimmune diseases
  • International normalized radio (INR), activated partial thromboplastin time (aPTT), and clotting time for coagulopathy
  • CBC and differential for infection
  • Thyroid-stimulating hormone (TSH) for thyroid disease
  • Fasting blood glucose for diabetes mellitus
  • Cholesterol and triglycerides for hyperlipidemia

Imaging Studies

• Approximately 1-2% of patients with ISSHL have internal auditory canal (IAC) or CPA tumors. Conversely, 3-12% of patients with vestibular schwannomas present with sudden hearing loss.
• Magnetic resonance imaging (MRI) with gadolinium diethylenetriamine-pentaacetic acid (DPTA) enhancement is the criterion standard test for diagnosing CPA masses, especially because a 30-40% false-negative rate exists with auditory brainstem response (if hearing levels permit). The cost issue for MRI has been addressed by performing limited studies using fast spin echo techniques.
• In young patients, for whom only a small possibility of detecting a vestibular schwannoma exists, a noncontrast temporal bone computed tomography (CT) scan could be obtained. Anatomic defects such as a Mondini dysplasia or enlarged vestibular aqueduct might account for a sudden hearing loss.

Other Tests

• Audiometry, including pure-tone and speech tests and immittance (tympanometry and acoustic reflex) tests, is mandatory. Testing can be directed by information gleaned from the history and physical examination. Obtaining those laboratory tests for which the results may influence the treatment plan is wise.
• Auditory brainstem response testing and otoacoustic emissions (OAE) tests may provide additional information regarding the functional integrity of the auditory system.
• • OAE testing can provide information about cochlear function, and the auditory brainstem response can be used to assess auditory nerve function.
  • The auditory brainstem response and OAE results may also assist in diagnosing a functional hearing loss.
• Vestibular tests are not mandatory and are obtained when indicated by the history and physical examination findings.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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 (Ni, 2004).
• 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 (Wei, 2006). 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 (Ho, 2005).Similar results were reported in yet another recent study (Gouveris, 2005). 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.

  Another recent study where the hyperbaric oxygen therapy consisted of exposure to 100% oxygen at a pressure of 250 kPa for a total of 60 minutes in a multiplace hyperbaric chamber concluded that hyperbaric oxygen therapy with high doses of glucocorticoids improves the results of conventional sudden sensorineural hearing loss treatment and should be recommended and that the best results are achieved if the treatment is started as early as possible (Narozny, 2004).

  Some authors 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 (Bennett, 2005).

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

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

No randomized controlled trial exists demonstrating efficacy of any medical therapy in ISSHL. Steroids and diuretics have been included here because they are relatively accessible, but this emphatically should not be taken as endorsement for the use of either.

Drug Category: Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Drug Category: Diuretics

Beneficial in the treatment of fluid retention.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Outpatient Care

• Patients who continue to have a significant hearing loss require aural rehabilitation.
  

Prognosis

• Fortunately, the spontaneous recovery rates for sudden sensorineural hearing loss are generally good. These rates range from 47-63%, with the caveat that different studies used different criteria for degrees of recovery. Ideally, criteria will be established by which to measure hearing improvement.
• Negative prognostic factors include the following:
• • Age younger than 15 years or older than 65 years
  • Elevated ESR (>25)
  • Vertigo or vestibular changes evident on ENG
  • Hearing loss in the opposite ear
  • Severe hearing loss
• Prognostic factors affecting outcome in patients with sudden sensorineural hearing loss have been postulated. Vertigo or imbalance seems to portend a lower recovery rate. Two studies, in addition, found severe vertigo associated with more cases of high-frequency or profound hearing loss. This association could be explained anatomically by the close proximity of the basal turn of the cochlea to the vestibule.
• Considerable controversy exists regarding the prognosis in sudden hearing loss. Existing studies have not provided answers to questions regarding spontaneous recovery rate, the best therapeutic regimen, prognostic factors in recovery, and the pathophysiology of sudden hearing loss. These are questions that require a randomized controlled clinical trial of adequate size. Given the apparent rate of spontaneous recovery, the prognosis for some hearing recovery for patients with sudden sensorineural hearing loss is moderate. Selection bias is likely to affect most studies of ISSHL because patients with sudden hearing loss and spontaneous recovery within a few days probably do not seek medical evaluation. The true spontaneous recovery rate is unknown.
• A review of outcomes for the various therapeutic regimens produces conflicting results, again because of differences in reporting. With different inclusion criteria, exclusion criteria, recovery criteria, and duration of follow-up, comparisons between studies are often not valid. Many studies lack control subjects.
• • Several studies using vasodilator therapy as a component of treatment did not show significant differences from placebo. However, in 1996, Fetterman et al reported their best recovery results (63% improved pure-tone average [PTA] by more than 10 dB or speech discrimination more than 15%) when treatment included vasodilators. Based on controlled studies, little data support vasodilator therapy.
  • Several studies assessing low molecular weight dextrans and/or pentoxifylline did not demonstrate recovery rates better than placebo. One exception by Redleaf et al in 1995 reported 64% of patients improving. In this study, concomitant diatrizoate therapy was also administered, and no placebo arm was used.
  • Corticosteroid therapy has been investigated with varying outcomes. Published recovery rates range from 41-61%. In 1980, Wilson et al demonstrated a significant improvement, finding 61% improved on oral corticosteroids compared to a 32% improvement rate on placebo. They also stratified their patient groups by audiometric patterns, and determined that hearing losses from 40-90 dB responded better to steroid therapy; 78% improved.
  • Diatrizoate has not been studied to any great extent. In 1987, Wilkins et al found no significant difference in recovery using diatrizoate in a multidrug regimen compared to spontaneous recovery rates. Redleaf et al reported a beneficial effect using diatrizoate and dextran, improving 64% of patients. Interestingly, using the hearing recovery criteria of Wilkins et al, recalculated data from the 1995 Redleaf study indicated only a 36% recovery rate to a classification of complete or good.
  • A review of hyperbaric oxygen therapy found a beneficial effect, especially if therapy was instituted within 2-6 weeks of the onset of the hearing loss. Fifty percent of patients improved by 20 decibels. If therapy was delayed, less improvement was found, with no beneficial effect for delays of longer than 3 months.

Patient Education

• Patients should be educated about the natural history of ISSHL.
• For excellent patient education resources, visit eMedicine's Ear, Nose, and Throat Center. Also, see eMedicine's patient education article Hearing Loss.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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Article Last Updated: Jun 16, 2006