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ORIGINAL ARTICLE
Ahead of print publication  

Evaluation and management of sudden sensorineural hearing loss in Indian naval scenario


1 ENT Specialist , Department of ENT, INHS Sanjivani, SNC, Kochi, Kerala, India
2 Marine Medicine Specialist, Department of Marine Medicine, Diving School, SNC, Kochi, Kerala, India
3 Consultant ENT Specialist, Department of ENT, Madras ENT Research Foundation, Chennai, Tamil Nadu, India

Date of Submission29-Feb-2020
Date of Decision14-Apr-2020
Date of Acceptance31-May-2020
Date of Web Publication16-Sep-2020

Correspondence Address:
Sunil Mathews,
INHS Sanjivani, SNC, Kochi, Kerala
India
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jmms.jmms_17_20

  Abstract 


Introduction: Sudden sensorineural hearing loss (SSNHL) is a medical emergency and if treated early, may improve chances of recovery of lost hearing. Delay in diagnosis and/or initiation of treatment may cause a permanent hearing loss. A relative lack of standardized management protocol has resulted in wide variation among various institutes for investigations and treatment of SSNHL. Aims and Objectives: To provide an overview of causes, methods of evaluation, and management of SSNHL pertaining to the Indian Naval scenario, based on cases evaluated and managed at a zonal level hospital of Indian Navy, over a period of 1 year. Materials and Methods: A prospective cohort study was conducted at the department of otorhinolaryngology at a zonal hospital of Indian Navy from January 2018 to December 2018 and subsequent follow-up until June 2019, giving a minimum follow-up of 6 months for each case. Ten cases were included in the study, evaluated, and managed and the outcomes were analyzed. Among these, six were idiopathic SSNHL (ISSNHL) cases and four were noise-induced (after small-arm firing) SSNHL cases. Results and Conclusion: Hearing outcomes were better and statistically significant for ISSNHL cases compared to noise-induced SSNHL cases. There was a strong negative correlation between the delay in initiation of treatment with improvement in hearing after treatment. The pattern of audiogram is a good predictor for recovery/no recovery, wherein flat and ascending types showed complete recovery, whereas descending type and profound hearing loss type showed no/partial recovery.

Keywords: Hyperbaric oxygen therapy, idiopathic, noise induced, steroid, sudden sensorineural hearing loss



How to cite this URL:
Mathews S, Dalawayi SS, Gangwar V, Vadivu AS. Evaluation and management of sudden sensorineural hearing loss in Indian naval scenario. J Mar Med Soc [Epub ahead of print] [cited 2020 Sep 19]. Available from: http://www.marinemedicalsociety.in/preprintarticle.asp?id=294289




  Introduction Top


Sensorineural hearing loss (SNHL) is an auditory dysfunction due to lesion of inner ear or auditory nervous system. There are three types of SNHL: sudden, progressive, or chronic.[1] SNHL is generally taken as air conduction (AC) threshold more than 25 dB (decibel) over 0.5, 1, 2, and 4 kHz (kilohertz).[2] Definition of sudden SNHL (SSNHL) is different from that of SNHL. There are several definitions for SSNHL. Although De Kleyn et al. gave first description of SSNHL in 1944, the most accepted definition is given by Wilson et al. According to them, SSNHL is defined as hearing loss of more than 30 dB at three or more contiguous frequencies developing over a period of three days or less.[3] The annual incidence of SSNHL is estimated to be 5–30 per 100,000 persons.[4],[5],[6] Among all cases of SSNHL, 99% of cases are unilateral.[7] There is a wide age distribution for SSNHL with an average of 50–60 years with no gender preference.[8] SSNHL is an otological emergency for which a definite etiology and treatment remains controversial. The etiology is identified in <5%–10% of cases. However, prompt recognition and management have shown to improve hearing outcomes.[9]

Historically, although many factors have been implicated as causes of hearing loss, the link for many of these factors with hearing loss has not been proven scientifically.[10] In most instances of SSNHL, although reliable diagnosis of the cause is impossible, there are many possible reasons implicated.[1] Possible causes to be considered in every case of SSNHL are listed as follows: (1) viral infections: mumps, measles, rubella, and varicella-zoster viruses are more probable causes whereas cytomegalovirus, adenovirus III, poliovirus, coxsackie virus, Epstein–Barr virus, human immunodeficiency virus (HIV), and herpes simplex are less probable causes; (2) bacterial infections: syphilis, suppurative labyrinthitis, and meningitis/encephalitis; (3) vascular causes: hemorrhage, arterial occlusion, and vasospasm; (4) autoimmune diseases: Wegener's granulomatosis, systemic lupus erythematosus, rheumatoid arthritis, Sjogren's syndrome, polyarteritis nodosa, relapsing polychondritis, ulcerative colitis, Cogan's syndrome, antiphospholipid syndrome, sarcoid, and autoimmune inner ear disease; (5) hypoxia; (6) ototoxic drugs; (7) neurologic causes such as multiple sclerosis, focal pontine ischemia, migraine; (8) Meniere's disease; (9) neoplastic causes such as vestibular schwannoma, meningioma, leukemia, and myeloma; (10) traumatic causes such as temporal bone trauma, noise trauma, barotrauma, perilymph fistula, and ear surgeries (stapedectomy); (11) psychogenic; and (12) nonorganic hearing loss (malingering).[1],[9]

Investigations are usually carried out to identify any of the possible causes as listed above, to provide specific management. Usual methods of treatment include systemic and/or intratympanic corticosteroid, antiviral therapy, hyperbaric oxygen therapy (HBOT), neurotropic vitamins, and so on. The aims and objectives of this study were to provide an overview of causes, methods of evaluation, and management of SSNHL pertaining to the Indian naval scenario, based on cases evaluated and managed at a zonal level hospital of Indian Navy, over a period of 1 year and subsequent follow-up.


  Materials and Methods Top


A prospective cohort study was conducted at a zonal hospital of Indian Navy for the evaluation and management of SSNHL cases. All the cases received at the Department of Ear, Nose, and Throat (ENT), from January 01, 2018, to December 31, 2018, were included in this study. Patients with acute or chronic otitis media and conductive/mixed hearing loss were excluded from this study. This hospital had received 12 cases of sudden hearing loss in a period of 1 year (2018). Among these 12 cases, two had associated perforation of the tympanic membrane with mixed hearing loss, hence were excluded from the study and the remaining ten cases with SSNHL were included in the study. Among these 10 cases, six were idiopathic sudden SNHL cases (ISSNHL) and four were noise-induced SSNHL cases. As all ISSNHL cases were unilateral, they constituted six ears to the study. Whereas, among four cases of noise-induced SSNHL, three were bilateral and one was unilateral; hence, this group constituted seven ears for the study. Hence, there were a total of 13 ears with SSNHL, which were included in the study. Informed consent was taken from the patients and ethical clearance was received from the institute.

After a detailed history taking, ENT, and systemic examination, all ISSNHL cases underwent the following investigations: serial pure-tone audiograms (PTA), complete blood count, packed cell volume, erythrocyte sedimentation rate (ESR), blood sugar levels (fasting and post prandial), fasting lipid profile, liver function test, renal function test, serum electrolytes, thyroid function test, venereal diseases research laboratory test, HIV test, urine analysis (routine and microscopy), and magnet resonance imaging (MRI) of brain and inner ear. Gadolinium-enhanced MRI of the brain, brainstem, and the internal auditory canals has the highest sensitivity for detecting retrocochlear pathology. The MRI protocol followed in the study center was to do a high-resolution 3-dimensional gradient echo or 3D fast-spin echo sequences (heavily T2-weighted sequences) and in case of any doubt or any positive findings, to go for gadolinium-enhanced T1-weighted MRI.

For noise-induced SSNHL cases, only serial PTA was done. All audiograms were taken using the same audiometer (Elkon EDA 3N3 mille) by the same audiologist in a sound-treated room and the hearing level was calculated by adding the AC thresholds (in dB) at 0.5, 1, 2, and 4 KHz and dividing the total by four. When the calculated value was below 25 dB, it was considered to be normal hearing; between 26 and 40 dB was considered 'mild SNHL'. Cases were included in the study, only if hearing loss was more than 30 dB at three or more contiguous frequencies as per the definition of SSNHL. AC threshold between 41 and 70 dB was defined as moderate hearing loss, between 71 and 90 dB as severe hearing loss, and above 90 dB as profound hearing loss. PTA was divided into ascending type, descending type, flat type, and profound hearing loss type, based on the appearance of the audiogram. Efficacy of treatment was defined according to PTA results after the treatment. Recovery was defined as improved average hearing threshold of at least 10 dB. Complete recovery indicated average hearing thresholds less than or equal to 25 dB or return to the hearing level before onset of hearing loss. Partial recovery referred to recovery not reaching the standard of complete recovery. If hearing gain was < 10 dB, it indicated“no recovery.” Time taken for onset of hearing loss, delay in reporting to ENT center and initiation of treatment, associated symptoms, and chronic illnesses, various treatment modalities provided and hearing levels before and after treatment were analyzed. Patients were offered the available treatment modalities in the hospital, such as systemic steroid, intratympanic steroid, HBOT, betahistine and neurotropic vitamins. Antiviral therapy was given only for ISSNHL cases. All patients were explained in detail regarding the urgency for initiation of treatment, risk of not recovering hearing if not treated promptly, and advantages and disadvantages of each mode of therapy. Patients who were unwilling for some modalities of treatment were not offered the same.

In this study, systemic corticosteroid was given as oral prednisolone 1 mg/kg body weight (after food), for 10 days and tapered over 21 days. Intratympanic steroid injection was performed under otomicroscopic guidance. After anesthetizing the external auditory canal and tympanic membrane by four-quadrant infiltration using 2% lignocaine with 1:200,000 adrenaline, 0.5 ml of dexamethasone (4 mg/ml) was injected into the middle ear using a 26G needle connected to 2 ml syringe, by“double-puncture method” where in one puncture is made in anterosuperior quadrant for efflux of air and another puncture in anteroinferior quadrant for injection of steroid [Figure 1]. In case of an anterior canal hump, punctures were given in the anterior most accessible part of tympanic membrane. Punctures were avoided in the posterosuperior quadrant to avoid accidental injury to incudostapedial joint and puncture in posteroinferior quadrant was avoided for preventing efflux of injected steroid through the puncture. Following injection, the patient's head was positioned at 45° angulation to opposite side and kept in that position for 40 min to ensure contact of injected steroid to round window membrane and, hence, diffusion into the inner ear. During this time, the patient was instructed not to swallow/chew or talk to prevent injected steroid escaping through eustachian tube into the nasopharynx. The ideal dose for intratympanic dexamethasone is 24 mg/ml (compounded) or 10 mg/ml (stock), if compounded concentration is unavailable. However, in our region of India, the only dose available was 4 mg/ml (available as 8 mg/2 ml ampoule), which was used in this study.
Figure 1: Intratympanic steroid injection in RT middle ear

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For HBOT, electrocardiography and chest X-ray (PA view) were taken, and if found normal, the patient was assessed by Marine Medicine Specialist and seated in hyperbaric oxygen chamber where he inhaled 100% oxygen for 1 h at 2.4 atmospheric pressure. Compression time for the chamber was 10 min and decompression time was 15 min [Figure 2] and [Figure 3]. The patient received one sitting per day (six sittings per week) for 10–20 sittings. After 10 sitting of HBOT, PTA was repeated, and if audiogram showed improvement in hearing, 10 more sittings of HBOT were given. If there was no improvement, further sessions were discontinued. These patients were followed up for a minimum period of 6 months, and clinical data was reviewed and analyzed.
Figure 2: Example of a hyperbaric chamber

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Figure 3: Patient seated inside a hyperbaric chamber

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  Results Top


The clinical details of the cases received are given in [Table 1]. The demographic profile, clinical findings, and inferences obtained are summarized in [Table 2]. Complete recovery of hearing was noted in 66.67% of cases of ISSNHL and 25% cases of noise-induced SSNHL; all these cases with complete recovery had a short duration of onset of symptoms from few minutes to 24 h, presented early, and were initiated with early treatment. A case of noise-induced SSNHL who presented 3 months after the onset showed no improvement in his hearing status, whereas others who presented within few days to few weeks showed some improvement in hearing (approximately 10–20 dB). MRI brain was done in all cases of ISSNHL and all studies were normal.
Table 1: Clinical summary of sudden sensorineural hearing loss cases reported at zonal naval hospital in 2018

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Table 2: Summary and interpretations of the clinical findings

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Since the data of this study were nonparametric, to compare the change in AC threshold before and after treatment, within each group, Wilcoxon signed-rank test was used, and to compare the outcome between the two groups, Mann–Whitney U test was used [Table 3]. To find out any correlation between the onset of SSNHL and delay in initiation of treatment, Pearson's correlation coefficient was used [Table 4].
Table 3: Statistical analysis of the data within the groups and between the two groups

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Table 4: Correlation between delay in start of treatment with hearing improvement after treatment

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  Discussion Top


One of the most commonly implicated causes for SSNHL is immune mediated. The clinical picture of immune-mediated SNHL is mostly characterized by bilateral, asymmetric SNHL, which is rapidly progressive, often associated with tinnitus and vestibular symptoms. It can progress fast and lead to severe bilateral SNHL in a few days to weeks. In rare cases, it presents as unilateral SSNHL and manifests in the contralateral ear after a variable period. The clinical significance of immune-mediated SNHL largely lies in the fact that it is one of the few SNHLs that may be reversible with early and adequate treatment.[11]

A vascular cause for ISSNHL is a popular theory because of the blood supply to the cochlea by an end artery and hence its susceptibility to damage by vascular occlusion. As per isolated case series, patients with sickle cell anemia and Waldenstrom's macroglobulinemia have a higher risk of SSNHL, but they are usually reversible with treatment.[12],[13] Studies have shown increased prevalence of hyperglycemia, hypercholesterolemia, and abnormal thyroid hormone levels in patients with cochlear and vestibular dysfunction, when compared to general population.[14],[15] Approximately 15% of vestibular schwannoma manifest with SSNHL and around 5% of the patients of SSNHL may have vestibular schwannoma.[1]

Exposure to intense noise can damage the cochlea and cause hearing loss. If the noise exposure is moderate (between 78 and 85 dB), it produces a temporary threshold shift (TTS), which, if the ear is allowed to rest, recovers. The mechanism behind the development of a TTS is metabolic exhaustion and recovery. If the sound is more intense, TTS can change into a permanent threshold shift (PTS), which is caused by the anatomical damage to the outer hair cells of cochlea. The point at which TTS changes to PTS is about 140 dB. In Military setup, even shooting on the range may produce hearing loss; up to 3% of recruits will receive a permanent measurable hearing loss from their first exposure to rifle practice, whereas others with 'tough' ears can shoot with impunity virtually all their life.[16]

The main options in the treatment for ISSNHL are systemic steroids, intratympanic steroid therapy, and vasodilator drugs.[3],[17] If there are inflammatory neural changes or presence of immunological diseases, systemic steroids are of help.[1] Steroids induce suppression of the immune response, change microcirculation, and decrease endolymphatic pressure. According to many authors, responsiveness of immune-mediated SSNHL happens in the initial days or weeks. Hence, it is important to initiate appropriate treatment at the earliest possible time to stop the progression of the lesion and for a better prognosis.[18],[19]

Intratympanic steroid injection therapy can be performed either directly by a hypothermic needle or after inserting a grommet. It can be offered as a primary therapy or can be combined with systemic steroid therapy or it can be given as a rescue therapy when systemic steroid therapy fails.[20] Intratympanic steroid therapy has the following advantages: it can be performed as an outpatient procedure under microscopic guidance; administration is easy; can be started soon after the diagnosis; relatively painless after local anesthesia; useful in patients in whom systemic corticosteroids are contraindicated (e.g.,: HIV, tuberculosis, uncontrolled diabetes, cataract, myasthenia gravis, and glaucoma); and achieves high localized drug concentration when administered directly on the affected ear. Usually, a total of three to five intratympanic injections are given, two or three injections a week. It can also be administered through a grommet inserted through the tympanic membrane. The rare risk of residual perforation and otitis media secondary to perforation after a grommet insertion should be discussed with the patient and informed consent taken. A recent study was conducted by Tang et al. comparing efficacy of systemic prednisolone therapy against rescue therapy with intratympanic dexamethasone injections, started after failure of systemic prednisolone, in cases of bilateral ISSNHL cases. They found significant difference in achieving complete or partial recovery in rescue therapy group (36.4% against 17.5%). They concluded that intratympanic injection of dexamethasone after failure of systemic prednisolone therapy was a better choice for simultaneous bilateral SSNHL compared to traditional systemic prednisolone only.[21] In an animal study conducted on adult rats to study the effects of intratympanic dexamethasone injection for ISSNHL, it was found that the maximum concentration of dexamethasone in the inner ear was achieved after 30 min of injection, as assessed by immunofluorescence of the inner ear specimens.[22] There are centers which give mega dose of systemic steroid for shorter duration (injection methylprednisolone 1 g loading dose intravenously immediately on admission followed by 500 mg twice daily for three days), followed by oral prednisolone in tapering dose over 2–3 weeks. Some centers start the intratympanic steroid injections along with the mega dose of systemic steroids or they start soon after the mega dose of steroids if there is no significant improvement in hearing levels.

HBOT in ENT is well established for some disorders such as ISSNHL, noise-induced hearing loss, acoustic trauma, tinnitus, malignant otitis externa, mucormycosis of paranasal sinuses, and skin flaps with compromised blood supply. The mechanism by which HBOT is useful for ear pathologies is the rise in partial pressure of oxygen in perilymph and endolymph in inner ear, which then diffuses and supplies oxygen to sensory cells of the inner ear. The rise in partial pressure of oxygen increases even up to 460% in labyrinthine fluids and it remains 60% above normal after 1 h of completion of therapy. In addition, HBOT also causes a reduction in hematocrit and decrease in the blood viscosity, which helps in improving diffusion of oxygen to cochlear and vestibular cells. In SSNHL, the results are better if the HBOT is started earlier than in those started late after 3 months.[23] The risk for middle ear barotrauma should be discussed with the patient before the start of HBOT and the patient should be assessed for signs of middle ear barotrauma after each session of HBOT.

In this study and as shown in other studies, the type of audiogram seems to be a good predictor for recovery wherein flat and ascending types showed complete recovery, whereas descending type and profound hearing loss type showed no or partial recovery. Some poor prognostic factors for hearing recovery in cases of SSNHL have been identified by various studies, and these include a raised ESR, presence of severe vertigo, old age (over 60 years), delayed presentation, and patients with profound hearing loss and a downward-sloping audiogram (descending type).[1],[9]

As per the guidelines by the American Academy of Otolaryngology-Head and Neck Surgery in 2019, strong recommendations for the clinicians are to (1) distinguish SNHL from hearing loss due to conductive causes; (2) patients with ISSNHL should be educated about the natural progression of the disease, risks and benefits of medical interventions, and limitations of existing evidence regarding efficacy of interventions; and (3) patients with residual hearing loss and/or tinnitus should be counseled about the possible benefits of audiological rehabilitation. Recommendations are made for the following: (1) cases of presumptive SSNHL be assessed for bilateral SSNHL, recurrent episodes of SSNHL, and/or focal neurological deficits; (2) in patients with sudden hearing loss, obtain audiometry as soon as possible (within 14 days of symptom onset) to confirm the diagnosis of SSNHL; (3) clinicians should evaluate patients with SSNHL for retrocochlear pathology by obtaining MRI or auditory brainstem response; (4) clinicians should offer intratympanic steroid therapy when patients have incomplete recovery from SSNHL, 2–6 weeks after onset of symptoms; and (5) clinicians should obtain follow-up audiometric evaluation within 6 months of completion of treatment. They offered the following options that clinicians may offer: (1) corticosteroids as initial therapy to patients with SSNHL within 2 weeks of symptom onset, (2) offer HBOT combined with steroid therapy within 2 weeks of onset of SSNHL, and (3) offer HBOT combined with steroid therapy as salvage therapy within 1 month of onset of SSNHL. Strong recommendations were made against the following: (a) in the initial evaluation of a patient with presumptive SSNHL, clinicians ordering for computed tomography scan of head/brain; (b) clinicians routinely prescribing thrombolytics, antivirals, vasodilators, vasoactive substances, or antioxidants; and (c) clinicians obtaining routine laboratory tests in patients with ISSNHL.[24] These guidelines may be followed by each clinician managing a case of SSNHL.

To summarize the study, review of literature and this study have shown that improvement in hearing is much better for cases of ISSNHL, compared to noise-induced cases. Most of the naval stations have the facility of HBOT, which is unique when compared to other services and civil centers. This facility should be utilized to benefit patients with SSNHL. Men and medical personnel should be educated to report cases of SSNHL at the earliest to nearest ENT center, so that chances of recovery is maximum. Delayed initiation of treatment has shown no or minimal recovery in hearing. Noise-induced SSNHL is an avoidable disability, if proper precautions are taken, such as wearing of properly fitted ear defenders during range firing, strict adherence to ear defenders when entering high-noise compartments such as engine room/flight deck, on board ship.

Limitations of this study are that, in cases of ISSNHL, about 32%–65% patients recover spontaneously, and the greater part of that recovery occurs in the first few weeks after onset. This fact in addition to the low incidence rate of SSNHL and less number of cases reported in a single center has made the validation of empirical treatments difficult.

Future recommendations are for genetic analysis of patients with SSNHL to find out their genetic susceptibility to develop SSNHL when compared to the general population.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
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Sanchez TG, Medeiros IR, Fassolas G, Coelho FF, Constantino GT, Bento RF. Frequency of glucose, lipids and thyroid hormones disorders in tinnitus patients. Arq Int Otorrinolaringol 2001;5:142-6.  Back to cited text no. 15
    
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Alberti P. Traumatic sensorineural hearing loss. In: Ludman H, Wright T, editors. Diseases of the Ear. 6th ed.. London: Hodder Arnold; 2006. p. 483-93.  Back to cited text no. 16
    
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Fetterman BL, Saunders JE, Luxford WM. Prognosis and treatment of sudden sensorineural hearing loss. Am J Otol 1996;17:529-36.  Back to cited text no. 17
    
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24.
Stachler RJ, Chandrasekhar SS, Archer SM, Rosenfeld RM, Schwartz SR, Barrs DM, et al. Clinical Practice Guideline: Sudden hearing loss. Otolaryngol Head Neck Surg 2019;161:S1-45.  Back to cited text no. 24
    


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