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ORIGINAL ARTICLE
Year : 2013  |  Volume : 19  |  Issue : 3  |  Page : 95-99

Update on the sudden hearing loss


Department of Head and Neck, Hospital of Cattinara, Trieste, Italy

Date of Web Publication2-Sep-2013

Correspondence Address:
Federica Bullo
Strada di Fiume 447, 34134 Trieste
Italy
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-7749.117462

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  Abstract 

Aims: Sudden hearing loss is defined as a sensory neural hearing deafness of at least 30 dB in three consecutive speech frequencies that as occurred within the 3 days. It is a medical emergency and the treatment should start as soon as possible; up to now therapies are empirically addressed to improve hearing. Materials and Methods: We have evaluated 558 patients with a diagnosis of sudden hearing loss. In our study, we have investigated possible prognostic factors of hearing loss and their influence on the recovery of the pathology. Results and Discussion: Sudden hearing loss requires an immediate therapeutic intervention. The corticosteroid therapy remains the most accredited one at which are reported the most satisfactory results. We have recognized as negative prognostic factors hearing loss on acute frequencies in the audiometric exam, the presence of a severe-deep hearing loss and a delay in starting therapy. Conclusion: The sudden hearing loss is an otologic emergency which requires an immediate therapeutic intervention. The most accredited therapy remains the corticosteroid therapy. Frequencies we have recognized as negative prognostic factors hearing loss on acute frequencies. The presence of a severe-deep hearing loss, and a delay in starting therapy.

Keywords: Carbogen, Corticosteroid therapy, Sudden hearing loss, Tinnitus, Vertigo


How to cite this article:
Bullo F, Tzamtzis S, Tirelli G. Update on the sudden hearing loss. Indian J Otol 2013;19:95-9

How to cite this URL:
Bullo F, Tzamtzis S, Tirelli G. Update on the sudden hearing loss. Indian J Otol [serial online] 2013 [cited 2019 Jun 18];19:95-9. Available from: http://www.indianjotol.org/text.asp?2013/19/3/95/117462


  Introduction Top


Sudden hearing loss is defined as a sensory neural hearing deafness of at least 30 dB in three consecutive speech frequencies that has occurred within 3 days. [1],[2] More than 90% of cases are unilateral. [3] The incidence of sudden hearing loss ranges from 5 to 20 cases per 100 with a peak in patients ages 50-60; [4] it affects both sexes equally. [5] Many patients with auditory loss may suffer also from tinnitus (60%) and vertigo (30-40%). [1] Despite scientific effort, the etiologic factors still remain uncertain.

There are many different theories in order to explain etiopathology of sensory neural hearing loss (SNHL): Circulatory disturbances, viral disease, autoimmune pathologies, temporary breaks of inner ear membranes or the combination of more than one of these. [6],[7]

Many authors consider SNHL an otologic emergency and the treatment should start as soon as possible; [3] up to now therapies are empirically addressed to improve hearing. It is difficult to evaluate the efficacy of therapies because up to 65% of patients may experience spontaneous recovery of pre loss hearing. [8]

In our study, we have investigated possible prognostic factors of hearing loss and their influence on the recovery of the pathology, such as the severity of hearing loss, the kind of audiogram curves, the presence of comorbidities, the time elapsed between onset of symptoms and beginning of therapy, and the different auditory outcome of three different treatment protocols.


  Materials and Methods Top


We have evaluated 558 patients who were diagnosed with SNHL at Head and Neck Department of Trieste between January 2007 and March 2012. All of them were more than 18 years old. Of this group, 282 patients are been included in our study. Instead, we have excluded all the patients who were diagnosed with Meniere disease, acoustic neuroma, or bilateral hearing loss. For all the included patients, we have evaluated following parameters: Demographic odds, presence of comorbidities (diabetes, hypertension, dyslipidemia, and cardiovascular disease), severity of hearing loss, the elapsed time between onset of hearing loss and beginning of treatment and, the last but not the least, therapy administered to evaluate their influence on hearing recovery.

We classified the severity of hearing loss in four different degrees: Light (for loss of 20-40 dB), medium (41-60 dB), moderate (61-70 dB), severe (71-90 dB), and deep (more than 90 dB of hearing loss).

Patients were divided into four groups according to the elapsed time between the onset of hearing loss and the beginning of the treatment: Within 7 days, between 8 days and 14 days, between 15 days and 21 days, and more than 21 days after symptoms onset.

Then we have divided our patients in three groups in accord to the therapeutic protocol administered: 172 patients treated with Deflazacort, Carbogen, and Dextran, 74 patients treated with Deflazacort and Carbogeno, and 36 patients treated with Dextran and Carbogen.

In the second group, we avoided use of Dextran because of hypertension; while in group three, we didn't administered Deflazacort because of diabetes. Therapeutic protocols are summarized in [Table 1].
Table 1: Therapies adopted

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To check the existence of a relationship between the final outcome of the hearing loss and the diverse prognostic factors considered were carried out by an individual statistic by the University of Studies of Trieste of the Tables of Contingency for every of the considered variables.

The chi-squared was then obtained from the Tables of Contingency: It was statistically significantly considered a P-value < 0.05.


  Results Top


We enrolled 282 patients in the study, 138 males and 144 women; the average age was 60 years old. In 128 patients we have found co-morbidities, ypertension, diabetes, and other cardiovascular and dysmetabolic disease The distribution of our sample is summarized in [Table 2].
Table 2: Parameters evaluated

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At the end of therapy, we had complete recovery in 107 patients (36.9%), a partial recovery (more than 10 dB) in 86 patients (30.5%), while we had no improvement in hearing loss in 92 (32.62%).

In order to emphasize a possible correlation between the outcome of the hearing loss and the above mentioned variables there were built contingency tables [see [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9] and [Table 10]]. From these tables it was extracted the P-value, which emphasized a correlation statistically significant among the outcome, the beginning of therapy (P-value = 0.008), the severity of hearing loss (P-value = 0.001), the type of interested frequencies (P-value = 0.01), and the presence of vertigo (P-value = 0.01). In our sample, we have not found a correlation between the final recovery and comorbidity, sex, and the therapy performed.
Table 3: Comorbidities

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Table 4: Time to start of therapy

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Table 5: Frequencies interested

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Table 6: Gravity of hearing loss

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Table 7: Sex

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Table 8: Type of therapy

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Table 9: Smoke

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Table 10: Vertigo

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  Discussion Top


The sudden hearing loss is characterized by a hearing decrement generally unilateral (more than 90%), [3] often associated with tinnitus (60% of cases) and vertigo (30-40% of cases). [1] The tympanic membrane results undamaged at otoscopy. The audiometric exam is important to emphasize the real hearing loss.

In an accurate Literature revision, most accredited causes of the sudden hearing loss seems to be: Viral diseases, vascular sclerosis of the micro-circulation in the inner ear, temporary breaks of the inner ear membranes, and immune-mediated reactions. [9],[10]

In 1944, De Kleyn was the first to signal as possible causes of a sudden loss a blood loss, acute and chronicle inflammations, traumatic fractures, multiple sclerosis, brain tumors, ototoxic drugs, embolism, hypercoagulability, and radiations. [4] Later, Gussen 1949 [11] followed by Fowler (1950) [12] and Sheibe (1956) [3] proposed as cause a vascular origin or a patology of the 8 th pair of cranial nerves. According to Lindsay and Zuidema (1950) [13] vascular patologies as blood loss and thrombosis damaging the inner ear could justify a sudden hearing loss. In 1957, Van Dishoeck and Bierman reported cases of patients with sudden hearing loss preceded by flu-like symptoms, highlighting the evidence of a possible viral cause for the hearing loss; [14] this hypothesis was also supported previously by Heller and Lindenberg in 1956, who published a study where an infection from the Herpes Zoster virus was found as cause of the sudden hearing loss. [15] Also, be an autoimmune pathogenesis has been evaluated: McCabe was the first to find a correlation between sudden hearing loss and Rheumatoid Arthritis, Lupus, Polyarteritis Nodosa in 1979. [16],[17],[18],[19]

Many studies emphasized association between sudden hearing loss and cardiovascular and dysmetabolic comorbidities such as hypertension, diabetes mellitus, and dyslipidemia in which was observed an involvement of the microcirculation of the internal ear. [20]

Penido et al., observed that the worst results were obtained in patients with diabetes mellitus, hypertension, and dyslipidemia. [21] Duck et al., Morizono and Paparella and Yan-Lin found worse final results of the sudden hearing loss in patients whom presented more associated comorbidities. [22],[23],[24] In a study carried on the histopathology of the temporal bone performed on autoptic findings of diabetic patients, Makishima and Tanaka found alterations caused by the peripheral nerves characterized by a thinning of the fibers and a lumen reduction of the vessels of the vascular stria. [25] Bachor et al., also performed studies on histological changes of the temporal bone concluding that the vascular alterations caused by the internal ear could be associated to a hearing deficit. [26] In our sample 45.4% of the subjects reported at the remote medical history the presence of comorbidities such as diabetes mellitus, hypertension, dyslipidemia, and other cardiovascular pathologies; it was not found, however, a correlation statistically significant between the final results of the hearing loss and the presence of comorbidities. As far as the auditory recovery is concerned, there is no difference in Literature between the male and the female sex. [5] Also, in our study, we did not highlighted a better progress in one of the two sexes although the two groups were homogeneously distributed. Other factors which were seen to be able to negatively influence the auditory recovery in the patients with sudden hearing loss are: Age of the patient, severity of the hearing loss and kind of audiogram curves. From our results, it was not found a worse recovery in elderly patients while better results were obtained in patients with an initial medium-moderate hearing loss compared to patients with a severe-deep hearing loss (P-value = 0.001); furthermore patients with low frequencies problems (250-500 Hz) met a better auditory recovery compared to the patients with pantonal hearing loss or localized to the acute frequencies (descending curve) (4000-8000Hz) (P-value = 0.01).

All therapies for SNHL are empirical as the etiopathogenesis of the sudden hearing loss still remains uncertain; furthermore, it was demonstrated high-rate of a spontaneous recovery, which could reach 65% of so to influence the final outcome. [8] Wilson found a significant recovery in patients, which did steroid therapy in comparison with a control group though from a literature revision, this evidence was never confirmed. [27] There are frequently used vasodilatator drugs for the hypothesis of a possible vascular cause involved in the origin of the sudden hearing loss even though their effectiveness was never proved with certainty. [1] The labyrinthine artery supplies the vestibulocochlear artery and the spiral artery of the modiolus, which provide the cochlear and the vestibular apparatus. The labyrinthine artery being a terminal one doesn't have collateral branches and the blood which comes from periferical vessels cannot compensate the blood flow of the internal ear. The efficiency of Carbogen inhalations (mixture composed of 95% O 2 and 5% CO 2 ) in the SNHL treatment was described by Fisch as having a vasodilator effect it was able to increase the blood flow at the level of the intracranial vessels and so at the level of the internal ear also. [28],[29] In another study, the use of vasoactive drugs (a combination of Dextran with Procaine) did not obtained better results in comparison with the placebo treatment. [30] Our study did not identify statistically significant evidence regarding different therapeutic schemes implemented. This could be due to the fact that, at the exclusion of the third group of patients treated with Dextran eventually associated with inhalations of Carbogen (36 patients) all others followed the corticosteroid therapy, this way loosing homogenous groups which followed different therapeutic schemes. Ahn et al., demonstrated that the steroid intratympanic injection offers the advantage of obtaining a drug concentrations inside of the ear, limiting the appearance of side effects which can appear by making a corticosteroid therapy through systemic circulation. [31] In another work, the efficiency of the intratympanic corticosteroid therapy was proved in the patients who did not meet a significant improvement after a previous corticosteroid systemic therapy. [32]

Another widely used treatment in the sudden hearing loss is the hyperbaric therapy: The hyperbaric oxygen was used for the first time in 1873. [33] Currently, the hyperbaric oxygen is an efficient therapy which can be used in many pathologies, for example in the severe anemia, in the gas gangrene, in the arterial gas embolism, CO poisoning, necrotizing infections, damage from radiations, chronic osteomyelitis and even in acute ischemic events among which the sudden hearing loss and the myocardial ischemic. [34] The hyperbaric therapy consists of 100% O 2 intermittent inhalations within a pressurized chamber between 1.5 atmospheres and 3.0 atmospheres. Its immediate effect is that of increasing the O 2 quantity in tissues. Lamm and Klimpel preceded by Appaix and Demard carried important studies on the advantages of the hyperbaric therapy in sudden hearing loss therapy by highlighting the increase of partial oxygen pressure at the level of the internal ear. [35]

In our clinic, the hyperbaric therapy was adopted as therapeutic scheme from few months only, therefore, seeing the minimum percentage of the patients treated through this procedure they were not recruited in our study as they would not give statistically significant results for lack of homogeneity of the sample.

Finally, another factor that affects the recovery is the elapsed time between the onset of hearing loss and the beginning of the treatment. In Literature, the best results in terms of recovery are the patients which begin the therapy within 7 days from the onset of hearing loss. [36] Even in our study, it was highlighted that the best results are obtained beginning the therapy within the first 2 weeks with a better recovery percentage within the first 7 days (P-value = 0.008).


  Conclusion Top


The sudden hearing loss is an otologic emergency which requires an immediate therapeutic intervention. Despite of numerous studies conducted, the efficacy of any specific treatment was not yet demonstrated even if the corticosteroid therapy remains the most accredited one at which are reported the most satisfactory results. In our study, we have recognized as negative prognostic factors hearing loss on acute frequencies in the audiometric exam, the presence of a severe-deep hearing loss, and a delay in starting therapy. The presence of comorbidities in our sample did not negatively influence the final recovery. However, other studies have to be performed to try to understand the real etiopathogenesis of SNHL to identify the appropriate therapy.

 
  References Top

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33.Jung S, Wermker K, Poetschik H, Ziebura T, Kleinheinz J. The impact of hyperbaric oxygen therapy on serological values of vascular endothelial growth factor (VEGF) and basic fibrobast growth factor (bFGF). Head Face Med 2010;6:29.  Back to cited text no. 33
    
34.Topuz E, Yigit O, Cinar U, Seven H. Should hyperbaric oxygen be added to treatment in idiopathic sudden sensorineural hearing loss? Eur Arch Otorhinolaryngol 2004;261:393-6.  Back to cited text no. 34
    
35.Lamm H, Klimpel L. Hyperbaric oxygen therapy in internal ear and vestibular disorder. Preliminary report. HNO 1971;19:363-9.  Back to cited text no. 35
    
36.Nasole E, Cucci L. L'ossigenoterapia iperbarica nell'ipoacusia improvvisa: Le evidenze della letteratura. Medicina subacquea e iperbarica 2008;2:19-23.  Back to cited text no. 36
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10]



 

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