Inserting Steroids Into the Tympanic Cavity Doesn't Alleviate Sudden Hearing Loss Symptoms

Sudden sensorineural hearing loss (SSNHL) cannot be linked to any specific medical disorder, yet it should be treated as a hearing emergency. This disorder occurs over a course of a few hours or days and may vary from a mild to a profound hearing impairment. The impairment has an estimated incidence of five to 20 cases per 100,000 population. However, its true incidence is not known, since there are patients that may not seek treatment due to the spontaneous recovery from sudden hearing loss.

Most scientists believe that the most common causes of sudden hearing loss can be attributed to viral infection, vascular occlusion, and intralabyrinthine membrane breaks. There is gathering experimental, histopathologic and clinical evidence, however, that viral inflammation is the most common cause of this disorder.

In the laboratory, rapid hearing loss has been produced experimentally in herpetic and cytomegaloviral labyrinthitis in guinea pigs. Clinical evidence for identifying viruses as the cause for sudden hearing loss includes a significantly higher rate of specific antibodies in patients with iSSNHL. In addition, cytomegalovirus, mumps, and rubeola viruses have been identified in the inner ear in patients with SSNHL.

Steroids are the preferred treatment for sudden hearing loss if it is believed to be of viral origin (oral corticosteroids have been effective). Systemic steroids have many potentially harmful side effects including adrenal suppression and aseptic necrosis of the hip. Animal studies suggest inserting the steroid through a tympanic route may avoid the systemic side effects associated with oral steroids.

This study investigated the potential benefit of intratympanic steroids in the treatment of sudden hearing loss. The results of this protocol were compared to the results using oral steroids, since the latter have proven effective in SSNHL treatment.

Researchers set out to prove that intratympanic steroids would improve hearing recovery in patients with SSNHL as compared to patients treated with oral steroids alone. The authors of "Intratympanic Steroid versus Oral Steroid Therapy for Idiopathic Sudden Sensorineural Hearing Loss" are Robert A. Battista, MD FACS, Assistant Professor, Courtney Garrett MD, and Carlos Esquivel MD, from the Northwestern University Medical School, Chicago; Stacie Hudgens, Research Statistician, Center on Outcomes, Research and Education, Evanston Northwestern Healthcare, all in Illinois. Their findings are to be presented at the American Academy of Otolaryngology--Head and Neck Surgery Foundation Annual Meeting and OTO EXPO, September 22-25, 2002, at the San Diego Convention Center, San Diego, CA.

Methodology: A prospective record review was conducted on patients with sudden hearing loss from November 1999 to March 2002. Patient preference dictated assignment to treatment arm (oral steroids alone: (Group 1) or intratympanic steroid perfusion: (Group 2). Patients selecting intratympanic steroid perfusion were provided the infusion alone or in conjunction with oral steroids. The oral steroids received by patients in Group 2 were given either prior to, or concurrent with, intratympanic treatment.

Steroids were injected into the middle ear space and allowed to perfuse the middle ear for 30 minutes with the injected ear in an upward position. The patient was asked not to swallow for the duration of perfusion in order to prevent passage of the solution into the eustachian tube. Steroid administration was performed on one to four separate occasions over the course of seven to 14 days. Hearing improvement was defined as a decrease in pure-tone average (PTA) of 10 dB or a 15% improvement in word recognition score (WRS).

Results: Forty-two patients met the criteria for sudden hearing loss. Two patients had insulin-dependent diabetes and reacted negatively to intratympanic dexamethasone. Therefore, 40 patients were used for evaluation. There was no significant difference between the two treatment groups in terms of duration of hearing loss. Group 2, however, had a significantly greater number of patients with vertigo and much worse initial hearing compared to Group 1. As a result, the prognosis for hearing recovery was much worse for Group 2 patients before the start of treatment.

None of the patients who chose oral steroid treatment alone had profound hearing loss. On the other hand, patients with profound hearing loss accounted for the majority (56 percent) of subjects who chose intratympanic treatment. These differences in initial hearing level between treatment groups prevented meaningful statistical comparison of hearing recovery.

This study failed to show relative hearing recovery using intratympanic therapy for SSNHL. This could be a resut of (1) iSSNHL may not be the result of viral inflammation; and (2) The incorrect corticosteroid or an improper dosage was used for treatment.

Conclusion: Absolute hearing improvement was not significantly greater for patients with SSNHL treated with intratympanic steroids compared to patients treated with oral steroids alone. Statistical comparison of relative hearing recovery could not be made between treatment groups due to the significant differences in initial hearing loss between groups. Patients who chose to participate in intratympanic steroid treatment suffered from more severe hearing loss than those patients who chose oral steroid therapy.

There was no significant hearing recovery for patients with profound SSNHL treated with intratympanic steroids when compared to reports of patients treated with oral steroids alone. More study is needed to determine the best treatment, dosage and method of delivery for sudden sensorineural hearing loss.