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Abstract
The aim of this study was to describe our experience with intratympanic (IT) steroid
treatment of sudden sensorineural hearing loss (SSNHL) after the failure of intravenous
(IV) steroid treatment and to examine the efficacy of this treatment.
Double-blind studies were conducted for the treatment of idiopathic sudden hearing loss (ISHL) with oral steroids. The condition was defined as not less than a 30-dB loss over three contiguous frequencies in three days or less. Follow-up audiograms were obtained four weeks and three months later. Specific audiologic guidelines for the assessment of hearing recovery were used to ensure objectivity. Steroids had a statistically significant effect on the recovery of hearing in patients with moderate hearing losses. The nature of the hearing loss and its susceptibility to improvement with steroid therapy lend support to the hypothesis that viral cochlitis is the primary cause of ISHL.
Autoimmune disease (e.g., Cogan syndrome) and other inflammatory inner ear diseases may ravage the labyrinth if not treated aggressively with antiinflammatory medication. Corticosteroids are the mainstay of treatment, yet, partly because of the existence of the blood-labyrinthine barrier, the ideal drug, dose, and route of administration are currently unknown. In the present study, we established cochlear fluid pharmacokinetic profiles of hydrocortisone, methylprednisolone, and dexamethasone in the guinea pig following oral, intravenous, and topical (intratympanic) administration. High-performance liquid chromatography was used to determine the drug concentrations, and comparisons were made with simultaneous pharmacokinetic profiles from blood and cerebrospinal fluid. Our findings demonstrated a much higher penetration of all three drugs into the cochlear fluids following topical application as compared with systemic administration, with methylprednisolone showing the best profile. The results suggested that intratympanic administration of corticosteroids might be more efficacious while avoiding high blood levels and therefore the deleterious side effects of systemic use. Thirty-seven patients with various inner ear disorders causing sensorineural hearing loss were subsequently treated using intratympanic corticosteroids, 20 with dexamethasone, and 17 with methlyprednisolone. Patients with immune-mediated hearing losses showed the best results, with notable improvement also seen in several cases of a "sudden deafness." No benefit was seen in patients with cochlear hydrops or those with sudden deterioration of a preexisting hearing loss. Three patients developed a transient otitis media related to the treatments, easily controlled with antibiotics. There were no cases of treatment-induced hearing loss and no permanent tympanic membrane perforations. Overall injection of intratympanic corticosteroids for the treatment of hearing loss in inner ear disorders appears to be both safe and highly effective for certain disorders. The concept of this technique is supported by animal experimental data. The findings from the present study warrant further clinical application and experimental investigation.
Intratympanic steroids are increasingly used in the treatment of inner ear disorders, especially in patients with sudden sensorineural hearing loss (SNHL) who have failed systemic therapy. We reviewed our experience with intratympanic steroids in the treatment of patients with sudden SNHL to determine overall success, morbidity, and prognostic factors. Intratympanic steroids have minimal morbidity and the potential to have a positive effect on hearing recovery in patients with sudden SNHL who have failed systemic therapy. The authors conducted a retrospective review. Patients presenting with sudden SNHL defined as a rapid decline in hearing over 3 days or less affecting 3 or more frequencies by 30 dB or greater who underwent intratympanic steroids therapy (24 mg/mL dexamethasone) were reviewed. Excluded were patients with Meniere disease, retrocochlear disease, autoimmune HL, trauma, fluctuating HL, radiation-induced HL, noise-induced HL, or any other identifiable etiology for sudden HL. Patients who showed signs of fluctuation of hearing after injection were excluded. Pretreatment and posttreatment audiometric evaluations including pure-tone average (PTA) and speech reception threshold (SRT) were analyzed. Patient variables as they related to recovery were studied and included patient age, time to onset of therapy, status of the contralateral ear, presence of diabetes, severity of HL, and presence of associated symptoms (tinnitus, vertigo). A 20-dB gain in PTA or a 20% improvement in SDS was considered significant. : Forty patients fit the criteria for inclusion in the study. The mean age of the patients was 54.8 years with a range from 17 to 84 years of age. Overall, 40% (n = 16) showed any improvement in PTA or SDS. Fourteen (35%) men and 26 (65%) women were included. Using the criteria of 20-dB improvement in PTA or 20% improvement in SDS for success, 27.5% (n = 11) showed improvement. The mean number of days from onset of symptoms to intratympanic therapy was 40 days with a range of 7 days to 310 days. A statistically significant difference was noted in those patients who received earlier injection (P = .0008, rank sum test). No patient receiving intratympanic dexamethasone after 36 days recovered hearing using 20-dB PTA decrease or a 20% increase in discrimination as criteria for recovery. Twelve percent (n = 5) of patients in the study had diabetes with 20% recovering after intratympanic dexamethasone (not significantly different from nondiabetics at 28.6%, Fisher exact test, P = 1.0). Comparison to other studies that used differing steroid type, concentration, dosing schedule, inclusion criteria, and criteria for success revealed, in many instances, a similar overall recovery rate. Difficulty in proving efficacy of a single modality is present in all studies on SNHL secondary to multiple treatment protocols, variable rates of recovery, and a high rate of spontaneous recovery. Forty percent of patients showed some improvement in SDS or PTA after treatment failure. When criteria of 20-dB PTA or 20% is considered to define improvement, the recovery rate was 27.5%. Modest improvement is seen with the current protocol of a single intratympanic steroid injection of 24 mg/mL dexamethasone in patients who failed systemic therapy. Dramatic hearing recovery in treatment failures was rarely encountered. No patient showed significant benefit from intratympanic steroids after 36 days when using this protocol for idiopathic sudden SNHL. If patients injected after 6 weeks are excluded from the study, the improvement rate increases from 26.9% to 39.3%. Earlier intratympanic injection had a significant impact on hearing recovery, although with any therapeutic intervention for sudden SNHL, early success may be attributed to natural history. If we further exclude seven patients treated with intratympanic steroids within 2 weeks of the onset of symptoms (i.e., study only those patients treated with intratympanic dexamethasone between 2 and 6 weeks after onset of symptoms), still, 26% improved by 20 dB or 20% SDS. The recovery rates after initial systemic failure are higher than would be expected in this treatment failure group given our control group (9.1%) and literature review. These findings indicate a positive effect from steroid perfusion in this patient population.
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