None, D. S. G. & None, D. R. S. (2022). Study of Clinical Profile of Patients with Sudden Onset Sensorineural Hearing Loss: A Cross-Sectional Analysis. Journal of Contemporary Clinical Practice, 8(2), 86-94.
MLA
None, Dr. Shweta Gupta and Dr. Ravi Shanker . "Study of Clinical Profile of Patients with Sudden Onset Sensorineural Hearing Loss: A Cross-Sectional Analysis." Journal of Contemporary Clinical Practice 8.2 (2022): 86-94.
Chicago
None, Dr. Shweta Gupta and Dr. Ravi Shanker . "Study of Clinical Profile of Patients with Sudden Onset Sensorineural Hearing Loss: A Cross-Sectional Analysis." Journal of Contemporary Clinical Practice 8, no. 2 (2022): 86-94.
Harvard
None, D. S. G. and None, D. R. S. (2022) 'Study of Clinical Profile of Patients with Sudden Onset Sensorineural Hearing Loss: A Cross-Sectional Analysis' Journal of Contemporary Clinical Practice 8(2), pp. 86-94.
Vancouver
Dr. Shweta Gupta DSG, Dr. Ravi Shanker DRS. Study of Clinical Profile of Patients with Sudden Onset Sensorineural Hearing Loss: A Cross-Sectional Analysis. Journal of Contemporary Clinical Practice. 2022 Jul;8(2):86-94.
Background: Sudden sensorineural hearing loss (SSNHL) is an otologic emergency characterized by rapid onset of hearing impairment, yet its clinical profile remains incompletely characterized across diverse populations. This study aimed to comprehensively evaluate the demographic characteristics, clinical presentations, audiometric patterns, and etiological factors in patients with SSNHL. Methods: A cross-sectional study was conducted on 104 patients diagnosed with SSNHL at a tertiary care teaching hospital. All patients underwent comprehensive evaluation including detailed history, otologic examination, pure-tone audiometry, and laboratory investigations for infectious, autoimmune, and vascular etiologies. Hearing recovery was assessed at three months using Siegel's criteria. Results: The mean age of patients was 46.2 ± 14.8 years, with a slight female preponderance (53.8%). Unilateral involvement was observed in 95.2% of cases. Tinnitus was the most common associated symptom (86.5%), followed by aural fullness (72.1%) and vertigo (41.3%). Profound hearing loss (>90 dB) was present in 28.8% of patients, with flat audiometric configuration being the most frequent pattern (42.3%). An identifiable etiology was established in 32.7% of cases, with infectious causes (15.4%) being most common, followed by vascular (8.7%) and autoimmune (5.8%) etiologies. Complete or partial recovery occurred in 58.7% of patients. Vertigo (OR 3.24, p=0.008), profound hearing loss (OR 4.12, p=0.002), and delayed presentation beyond seven days (OR 2.86, p=0.01) were independent predictors of poor recovery.
Conclusion: SSNHL presents with heterogeneous clinical profiles, with most cases remaining idiopathic. Associated symptoms, severity of hearing loss, and timely presentation significantly influence outcomes. A systematic diagnostic approach enables etiological identification in one-third of cases, facilitating targeted management.
Keywords
Sudden sensorineural hearing loss
Clinical profile
Audiometry
Tinnitus
Prognosis.
INTRODUCTION
Sudden sensorineural hearing loss (SSNHL) is an otologic emergency characterized by rapid-onset hearing impairment of at least 30 dB affecting three or more contiguous frequencies within 72 hours.1 This condition represents a significant clinical challenge due to its abrupt presentation, potential for permanent disability, and profound impact on patients' communication abilities, social interactions, and psychological well-being.2 The sudden nature of hearing loss, often noticed upon awakening or developing over hours, creates substantial distress as patients confront the unexpected alteration of a fundamental sensory experience.3
The global incidence of SSNHL ranges from 5 to 77 per 100,000 individuals annually, with peak occurrence in the 40-60 years age group, though it can affect individuals across the entire age spectrum.4 The true incidence may be underestimated due to spontaneous recovery in mild cases and underreporting.5 Despite extensive research spanning several decades, the exact pathophysiology remains incompletely understood, and a definitive etiology is established in only 10-30% of cases, leading to the designation "idiopathic" for the majority of patients.6
Several pathogenic mechanisms have been proposed for SSNHL. The viral hypothesis suggests that viral infections—particularly reactivation of neurotropic viruses such as herpes simplex virus type 1, varicella-zoster virus, and Epstein-Barr virus—can directly invade the cochlea or induce inflammatory responses that damage the delicate hair cells of the organ of Corti.7 This is supported by temporal associations with upper respiratory infections and demonstration of viral DNA in cochlear tissues.8 The vascular theory posits that the cochlea's unique blood supply from the labyrinthine artery, an end-artery without collateral circulation, renders it vulnerable to ischemic events from thromboembolism, vasospasm, or hypercoagulable states.9 Autoimmune mechanisms have been implicated in patients with bilateral involvement or associated systemic autoimmune disorders, supported by responsiveness to immunosuppressive therapy⁽¹⁰⁾. Other proposed mechanisms include intracochlear membrane rupture and retrocochlear pathology such as vestibular schwannoma.11
Clinically, SSNHL typically presents with unilateral hearing loss in over 95% of cases, accompanied by tinnitus (70-90%), aural fullness (40-80%), and vertigo (30-50%).12 The presence of vertigo is thought to reflect more extensive labyrinthine involvement and carries adverse prognostic implications.13 Audiometric evaluation is essential for diagnosis and reveals variable severity ranging from mild to profound loss, with various configurations including low-frequency ascending, high-frequency descending, flat, and profound patterns.14 Flat and profound configurations generally portend worse outcomes compared to other patterns.15
Despite advances in diagnostic technology, significant knowledge gaps persist regarding relationships between clinical presentation, etiological factors, and outcomes. Furthermore, regional variations in demographic characteristics, genetic susceptibility, prevalence of infectious diseases, cardiovascular risk factor profiles, and healthcare-seeking behaviors necessitate population-specific data to guide clinical decision-making.16 In the Indian subcontinent, where healthcare infrastructure varies and the burden of cardiovascular risk factors such as diabetes and hypertension is rising, understanding the clinical profile of SSNHL in the local population assumes particular importance.
This study was therefore undertaken to comprehensively evaluate the demographic characteristics, clinical presentations, audiometric patterns, etiological factors, and short-term outcomes in 104 patients with SSNHL at a tertiary care center in India, with the goal of providing clinically relevant insights for diagnostic protocols, treatment strategies, and prognostic counseling in our population.
MATERIALS AND METHODS
Study Design, setting & population
A hospital-based cross-sectional observational study was conducted to evaluate the clinical profile of patients presenting with sudden onset sensorineural hearing loss. The study was conducted in the Department of Otorhinolaryngology at a tertiary care teaching hospital in India over an 12-month period. The hospital serves as a major referral center for a population of approximately 10 million people. The target population consisted of all patients aged 18 years and above presenting with sudden onset sensorineural hearing loss attending the outpatient department or emergency services of the study institution.
Inclusion criteria:
• Patients aged ≥18 years
• Diagnosis of SSNHL (≥30 dB hearing loss affecting ≥3 contiguous frequencies within 72 hours)
• Presentation within 30 days of symptom onset
• Willingness to provide informed consent
Exclusion criteria:
• Conductive or mixed hearing loss
• Previous hearing loss in affected ear
• History of ear surgery, trauma, or barotrauma
• Known middle ear pathology
• Noise-induced hearing loss
• Contraindications to corticosteroids
• Pregnancy or lactation
• Incomplete data or loss to follow-up
Sample Size Calculation
Sample size was calculated based on reported prevalence of tinnitus (80%) in SSNHL patients. With 95% confidence interval and 8% absolute precision, the minimum required sample size was 96 patients. Accounting for attrition, 110 patients were enrolled, and 104 completed all study procedures.
Procedure for Data Collection
Screening and Enrollment
All patients presenting with sudden hearing loss were screened for eligibility. Written informed consent was obtained from eligible participants.
Clinical Evaluation
A comprehensive history was obtained using a standardized case record form. Complete otologic examination including otoscopy, otomicroscopy, and tuning fork tests was performed. Neurological and vestibular assessments were conducted as indicated.
Audiometric Evaluation
Pure-tone audiometry was performed within 72 hours of presentation using a calibrated audiometer. Hearing loss severity and audiometric configurations were classified according to standard criteria.
Laboratory Investigations
Within two weeks of diagnosis, the following investigations were performed:
• Infectious disease screening (HSV, VZV, EBV, CMV, Borrelia)
• Autoimmune screening (ANA, anti-dsDNA, RF, ANCA, ESR, CRP)
• Vascular and coagulation profile (CBC, PT, aPTT, fibrinogen, protein C/S, homocysteine, anticardiolipin antibodies)
• Metabolic evaluation (fasting blood glucose, HbA1c, lipid profile, thyroid function tests)
Imaging Studies
All patients underwent HRCT of temporal bones. MRI with gadolinium was performed in patients with suspected retrocochlear pathology or neurological symptoms.
Treatment Protocol
All patients received oral prednisolone (1 mg/kg/day, maximum 60 mg/day) for 7-14 days followed by a tapering course. Intratympanic steroid injections were offered as salvage therapy.
Outcome Assessment
Hearing recovery was assessed at three months using repeat pure-tone audiometry and classified according to Siegel's criteria.
Statistical analysis
Data were entered into Microsoft Excel and analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± SD or median with interquartile range. Categorical variables were presented as frequencies and percentages. A p-value <0.05 was considered statistically significant.
RESULTS
Table 1: Demographic and Clinical Characteristics of Patients with SSNHL (N=104)
Characteristic Number Percentage
Age group (years)
18-40 33 31.7%
41-60 38 36.5%
>60 33 31.7%
Mean age ± SD (years) 46.2 ± 14.8
Sex
Male 48 46.2%
Female 56 53.8%
Laterality
Unilateral 99 95.2%
Bilateral 5 4.8%
Mean duration at presentation ± SD (days) 6.4 ± 4.2
Associated symptoms
Tinnitus 90 86.5%
Aural fullness 75 72.1%
Vertigo/dizziness 43 41.3%
Comorbidities
Hypertension 36 34.6%
Diabetes mellitus 28 26.9%
Dyslipidemia 22 21.2%
Smoking 24 23.1%
A total of 104 patients with sudden sensorineural hearing loss were included in the study. As shown in Table 1, the mean age was 46.2 ± 14.8 years, with the highest proportion (36.5%) in the 41-60 years age group. There was a slight female preponderance (53.8%). Unilateral involvement was observed in 95.2% of patients, with right ear involvement (50.0%) being slightly more common than left ear (45.2%). The mean duration from symptom onset to presentation was 6.4 ± 4.2 days, with only 39.4% presenting within the first 3 days. Tinnitus was the most common associated symptom (86.5%), followed by aural fullness (72.1%) and vertigo (41.3%). Among comorbidities, hypertension (34.6%) was most frequent, followed by diabetes mellitus (26.9%) and dyslipidemia (21.2%).
Table 2: Audiometric Findings at Presentation (N=104)
Parameter Number Percentage
Severity of hearing loss
Mild (26-40 dB) 12 11.5%
Moderate (41-55 dB) 18 17.3%
Moderate-severe (56-70 dB) 20 19.2%
Severe (71-90 dB) 24 23.1%
Profound (>90 dB) 30 28.8%
Mean PTA ± SD (dB) 68.4 ± 22.6
Audiometric configuration
Flat 44 42.3%
High-frequency descending 26 25.0%
Low-frequency ascending 18 17.3%
Profound (all frequencies) 16 15.4%
Table 2 summarizes the audiometric findings. The mean pure-tone average at presentation was 68.4 ± 22.6 dB. Profound hearing loss (>90 dB) was the most common severity category (28.8%), followed by severe loss (23.1%). Flat audiometric configuration was the most frequent pattern (42.3%), followed by high-frequency descending (25.0%), low-frequency ascending (17.3%), and profound patterns (15.4%).
Table 3: Etiological Profile of SSNHL (N=104)
Etiological Category Number Percentage
Infectious 16 15.4%
Vascular 9 8.7%
Autoimmune 6 5.8%
Otological 3 2.9%
Total identified etiologies 34 32.7%
Idiopathic 70 67.3%
As presented in Table 3, a potential etiology was identified in 34 patients (32.7%), while 70 patients (67.3%) were classified as idiopathic. Infectious causes were most common (15.4%), with HSV-1 being the most frequently identified pathogen. Vascular etiologies were found in 8.7%, autoimmune causes in 5.8%, and otological causes in 2.9% of patients.
Table 4: Hearing Outcomes at Three Months (Siegel's Criteria) (N=104)
Outcome Category Number Percentage
Favorable outcome 61 58.7%
- Complete recovery 27 26.0%
- Partial recovery 34 32.7%
Unfavorable outcome 43 41.3%
- Slight recovery 22 21.2%
- No improvement 21 20.2%
At three-month follow-up, hearing recovery was assessed using Siegel's criteria (Table 4). Favorable outcome (complete or partial recovery) was achieved in 61 patients (58.7%). Complete recovery was observed in 27 patients (26.0%), partial recovery in 34 patients (32.7%), slight recovery in 22 patients (21.2%), and no improvement in 21 patients (20.2%).
Table 5 compares factors between favorable and unfavorable outcome groups. Patients with unfavorable outcome were significantly older (51.6 vs. 42.4 years, p=0.001) and more likely to present after 7 days (41.9% vs. 18.0%, p=0.008). Vertigo was present in 58.1% of the unfavorable group compared to 29.5% of the favorable group (p=0.003). Profound hearing loss was more common in the unfavorable group (44.2% vs. 18.0%, p=0.004). Diabetes mellitus was also associated with poor outcome (37.2% vs. 19.7%, p=0.02). Flat and profound audiometric patterns were associated with poorer prognosis, while low-frequency ascending pattern had the best outcome (p=0.01).
Table 5: Factors Associated with Hearing Outcome (N=104)
Variable Favorable Outcome (n=61) Unfavorable Outcome (n=43) p-value
Age (years, mean ± SD) 42.4 ± 15.1 51.6 ± 13.2 0.001
Presentation >7 days 11 (18.0%) 18 (41.9%) 0.008
Vertigo present 18 (29.5%) 25 (58.1%) 0.003
Profound hearing loss 11 (18.0%) 19 (44.2%) 0.004
Diabetes mellitus 12 (19.7%) 16 (37.2%) 0.02
Audiometric pattern 0.01
- Low-frequency ascending 15 (24.6%) 3 (7.0%)
- High-frequency descending 17 (27.9%) 9 (20.9%)
- Flat 22 (36.1%) 22 (51.2%)
- Profound 7 (11.5%) 9 (20.9%)
Table 6: Multivariate Predictors of Unfavorable Outcome
Variable Odds Ratio 95% Confidence Interval p-value
Vertigo (present vs. absent) 3.24 1.36 - 7.72 0.008
Profound hearing loss (>90 dB) 4.12 1.68 - 10.11 0.002
Delayed presentation (>7 days) 2.86 1.25 - 6.54 0.01
Multivariate analysis (Table 6) identified three independent predictors of unfavorable outcome: vertigo (OR 3.24, 95% CI 1.36-7.72, p=0.008), profound hearing loss (OR 4.12, 95% CI 1.68-10.11, p=0.002), and delayed presentation beyond seven days (OR 2.86, 95% CI 1.25-6.54, p=0.01).
DISCUSSION
This study provides a comprehensive analysis of the clinical profile of 104 patients with sudden sensorineural hearing loss in an Indian tertiary care setting. The mean age of 46.2 years in our cohort aligns closely with the established understanding that SSNHL peaks in the fifth and sixth decades of life, consistent with large epidemiological studies reporting increased incidence with advancing age.4 The slight female preponderance (53.8%) is consistent with some studies, though others have described equal sex distribution.1 Unilateral involvement in 95.2% of patients corroborates the well-established pattern that SSNHL is typically a unilateral condition.7
The high prevalence of tinnitus (86.5%) in our patients aligns closely with the 70-90% range reported in previous studies.1,2 Aural fullness, reported by 72.1% of patients, is comparable to the prevalence reported by Aldè et al. in their study of young adults with SSNHL⁽¹⁾. This symptom warrants attention as it may lead to initial misdiagnosis as eustachian tube dysfunction, potentially delaying appropriate referral.3 The prevalence of vertigo (41.3%) falls within the 30-50% range documented in the literature.2 Importantly, our analysis confirms the adverse prognostic significance of vertigo, with 58.1% of patients in the unfavorable outcome group experiencing vertigo compared to only 29.5% in the favorable group (p=0.003). This finding is strongly supported by studies that identified dizziness as a prominent negative predictive factor for recovery.2,13 The presence of vertigo likely reflects more extensive labyrinthine involvement, affecting both cochlear and vestibular end-organs.13
The distribution of hearing loss severity revealed that profound loss (>90 dB) was the most common category (28.8%), with profound loss independently associated with poor recovery (OR 4.12, p=0.002). The mean pure-tone average of 68.4 ± 22.6 dB is comparable to previous reports.1 Flat audiometric configuration was most frequent (42.3%), followed by high-frequency descending (25.0%), low-frequency ascending (17.3%), and profound patterns (15.4%). The prognostic gradient observed—low-frequency ascending having the best prognosis (83.3% recovery), followed by high-frequency descending (65.4%), flat (50.0%), and profound patterns (43.8%)—aligns with established understanding that configuration reflects the extent of cochlear involvement.15 This finding is strongly corroborated by studies demonstrating that hearing recovery differs significantly according to audiogram configuration, with upsloping patterns showing the best outcomes while flat and downsloping curves were associated with poorer recovery.4,14
A potential etiology was identified in 32.7% of patients, exceeding the 10-30% range typically cited, reflecting our comprehensive diagnostic protocol. Previous studies have reported identification of specific causes in varying proportions, with otological, infectious, autoimmune, and vascular etiologies being documented.1,6 Infectious causes (15.4%) constituted the largest identifiable category in our series, supporting the viral hypothesis of SSNHL pathogenesis.7 Vascular etiologies (8.7%) highlight the importance of considering hypercoagulable states, particularly in younger patients without cardiovascular risk factors.9
The overall favorable outcome rate of 58.7% is comparable to previously reported recovery rates of 50-65%.2,4 The observation that 20.2% experienced no improvement highlights the need for continued research into more effective therapies.6 Three independent predictors of unfavorable outcome were identified: vertigo (OR 3.24), profound hearing loss (OR 4.12), and delayed presentation beyond seven days (OR 2.86). The association between delayed presentation and poor outcomes is well-established in literature.2,3 Recovery rates declined from 70.7% in patients presenting within 3 days to only 25.0% in those presenting after 15 days, reinforcing the emergency nature of SSNHL and the critical window for intervention.4,6 The adverse prognostic impact of diabetes mellitus observed in our univariate analysis (p=0.02) aligns with studies demonstrating that comorbidities including diabetes significantly impact therapeutic efficacy in SSNHL.5,9
The 4.8% with bilateral involvement in our study had notably poorer outcomes compared to unilateral cases, consistent with literature reporting lower recovery rates in bilateral SSNHL compared to unilateral cases.5,11 This disparity underscores the generally poorer prognosis associated with bilateral involvement.
Our findings have several clinical implications. First, the high prevalence of associated symptoms should prompt consideration of SSNHL even when hearing loss is not the primary complaint. Second, vertigo, profound hearing loss, and delayed presentation should inform early counseling regarding expected outcomes. Third, comprehensive diagnostic workup is warranted, particularly in patients with atypical features or bilateral involvement. The strong prognostic value of audiometric configuration, corroborated by Gallus et al.4, suggests this readily available parameter should be routinely incorporated into prognostic assessments.
This study has limitations including single-center design, three-month follow-up which may not capture late improvements, and lack of a control group. Future research should focus on multicenter prospective studies with longer follow-up, development of predictive models incorporating clinical and laboratory parameters, and investigation of genetic susceptibility factors and biomarkers of recovery such as the neutrophil-to-lymphocyte ratio associations identified by Gallus et al.4
REFERENCES
1. Aldè M, Di Berardino F, Marchisio P, Cantarella G, Zanetti D. Sudden sensorineural hearing loss in children and adolescents: clinical characteristics and outcome. Int J Pediatr Otorhinolaryngol. 2019;116:138-142. doi:10.1016/j.ijporl.2018.10.035
2. Nordlie E, Brannström KJ, Karltorp E, et al. Prognostic factors for recovery in sudden sensorineural hearing loss: a systematic review. Eur Arch Otorhinolaryngol. 2020;277(5):1305-1316. doi:10.1007/s00405-020-05847-6
3. Rauch SD. Idiopathic sudden sensorineural hearing loss. N Engl J Med. 2008;359(8):833-840. doi:10.1056/NEJMcp0802129
4. Stachler RJ, Chandrasekhar SS, Archer SM, et al. Clinical practice guideline: sudden hearing loss. Otolaryngol Head Neck Surg. 2012;146(3 Suppl):S1-S35. doi:10.1177/0194599812436449
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6. Chandrasekhar SS, Tsai Do BS, Schwartz SR, et al. Clinical practice guideline: sudden hearing loss (update). Otolaryngol Head Neck Surg. 2019;161(1 Suppl):S1-S45. doi:10.1177/0194599819859885
7. Kuhn M, Heman-Ackah SE, Shaikh JA, Roehm PC. Sudden sensorineural hearing loss: a review of diagnosis, treatment, and prognosis. Trends Amplif. 2011;15(3):91-105. doi:10.1177/1084713811408349
8. Merchant SN, Durand ML, Adams JC. Sudden deafness: is it viral? ORL J Otorhinolaryngol Relat Spec. 2008;70(1):52-60. doi:10.1159/000111048
9. Lin RJ, Krall R, Westerberg BD, Chadha NK, Chau JK. Systematic review and meta-analysis of the risk factors for sudden sensorineural hearing loss in adults. Laryngoscope. 2012;122(3):624-628. doi:10.1002/lary.22480
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11. Sauvaget E, Kici S, Kania R, Herman P, Tran Ba Huy P. Sudden sensorineural hearing loss as a revealing symptom of vestibular schwannoma. Acta Otolaryngol. 2005;125(6):592-595. doi:10.1080/00016480510028465
12. Nosrati-Zarenoe R, Arlinger S, Hultcrantz E. Idiopathic sudden sensorineural hearing loss: results drawn from the Swedish national database. Acta Otolaryngol. 2007;127(11):1168-1175. doi:10.1080/00016480701242468
13. Byl FM Jr. Sudden hearing loss: eight years' experience and suggested prognostic table. Laryngoscope. 1984;94(5 Pt 1):647-661. doi:10.1288/00005537-198405000-00009
14. Gallus R, Melis P, Rizzo D, et al. Audiometric patterns and prognostic factors in patients with sudden sensorineural hearing loss. Acta Otorhinolaryngol Ital. 2020;40(3):208-215. doi:10.14639/0392-100X-N0415
15. Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol Rhinol Laryngol. 1977;86(4 Pt 1):463-480. doi:10.1177/000348947708600406
16. Alexander TH, Harris JP. Incidence of sudden sensorineural hearing loss. Otol Neurotol. 2013;34(9):1586-1589. doi:10.1097/MAO.0000000000000222
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