Sensori-neural Hearing Loss (SNHL) Size of the problem WHO (2005) • 278 million with disabling hearing impairment • Disabling-moderate (41 d B +) or worse • 364 million- mild hearing impairment • 80 percent in low or middle income countries • Among 20 leading global burden of the disease Recent Increase is due to • Improved diagnosis and early detection • Longer survival of elderly • Increase in NIHL • Increase in ototoxicity
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Bhattarai sir sensorineural hearing loss - mbbs 2010
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Sensori-neural Hearing Loss (SNHL)Size of the problem WHO (2005)
• 278 million with disabling hearing impairment• Disabling-moderate (41 d B +) or worse• 364 million- mild hearing impairment• 80 percent in low or middle income countries• Among 20 leading global burden of the disease
Recent Increase is due to• Improved diagnosis and early detection• Longer survival of elderly• Increase in NIHL• Increase in ototoxicity
Sensori-neural Hearing Loss
Importance—profound effect On individuals
• Hinder speech, language and cognitive skill development in pre-lingual children
• Slow progress in schools• Difficulty in obtaining, keeping and performing in any
occupation• Significant social isolation and stigmatization- poor
interpersonal developmentSocial and economic
• Substantial cost of treatment and rehabilitation • Loss of productivity
Causes of SNHL
A. CongenitalGenetic
SyndromicNon-Syndromic
Non-genetic (Embryopathies)B. Acquired
Causes of SNHL
Congenital-Genetic (Hereditary) SNHL-SyndromicWaardenburg’s-White forelock, heterochromia of irisUsher- with retinitis pigmentosaAlport’s- with nephritisPendred- with hypothyroidismMarfan- skeletal defectsJervill –Lange- with abnormal EEG
• Mechanism-effect on sensory neuro-epithelium of the inner ear especially outer hair cells of the organ of Corti and type I hair cells of Crista ampulli
Aminoglycosides
• Widely used because potent and cheap• Still used in drug resistance tuberculosis, neonatal sepsis
• In 1-5% of patients exposed• Factors influencing-dose, duration, liver and kidney disease, bacteremia, concomitant use of other agents, genetic predisposition
• Some are cochleotoxic, some vestibulotoxic
Cytotoxic Agents
Cisplatin, carboplatin • Effective in solid head and neck squamous cell carcinoma• Highly ototoxic in about 50 % of patients but the exposed population is low• Loss of mainly outer hair cells
Loop Diuretics
Frusemide , ethacrynic acid, bumetanide•Moderate to low percent of population at risk•Mechanism
Reversible reductions of endocochlear potential
Electrolyte changes in inner ear fluidsHistologic changes in stria vascularis
Industrial Chemicals
• Toluene-used in printing and wood finishing,• Benzene- used in plastic industry
Permanent hearing loss in animals but inconclusive evidence in man
Polypeptide Antibiotics
Vancomycin, Viomycin• Not aminoglycosides• Less commonly used and less toxic • Ototoxic when given at higher doses for longer period of time
Macrolides
Erythromycin, azithromycin, clarithromycin• Transient ototoxicity when used in high doses• Reduction in transient evoked otoacoustic emissions
Salicylates
• Used for their anti-inflammatory, antipyretic, analgesic and antiplatelet effects
• In low doses protect inner ear from gentamicin induced ototoxicity but ototoxic in higher doses
Quinine Derivatives
• Widely used as antimalarial • Exposed population at risk very high
Ototoxicity
Clinical features• Tinnitus often the first symptom• SNHL-high tone more than low ones• Vertigo and disequilibrium• Oscillopsia- with aminoglycosides
Inability to focus sharply and jumping of the distant objects
Ototoxicity
Prevention and Treatment1. Avoidance of ototoxic agents as far as practicable2. Careful monitoring and early recognition3. Cessation of treatment and substitution by a different
agent4. SNHL-hearing aid5. Tinnitus-if disturbing-mild hypnotic and tinnitus masker6. Vertigo and disequilibrium –reassurance with
physiotherapy and head exercises
Presbyacusis
• New terminology--- age related sensori-neural hearing impairment
• Result of aging process and inevitable• Sixth decade onwards, if genetic predisposition and NIHL
Histopathological changes in the inner ear• Sensory-Hair cell degeneration and loss• Neural-degeneration of neurons and ganglions• Metabolic-Degeneration of stria vascularis• Mechanical-degeneration of supporting cells, membranes
Presbyacusis
Clinical features• Hearing impairment – slow and insidious, lack of clarity than loss of volume• “Don’t shout, I’m not deaf”• Tinnitus often the presenting symptom and sometimes may be troublesome
Presbyacusis
Management• Speaking in a clear and articulated voice close to the patients ear• Hearing aid- but in some amplification may not help
Noise induced hearing Loss (NIHL)
Reduction in auditory acuity associated with noise exposure --social, recreational, occupational
Types• Temporary threshold shift (TTS)- Lasting hours to days, reversible
• Permanent threshold shift (PTS) - Irreversible• Acoustic trauma- When a single exposure to intense trauma leads to immediate hearing loss
Noise induced hearing Loss (NIHL)
Pathology- various hypothesisMetabolic changes- TTS
Excessive glutamase release, cochlear hypoxia
Structural changes –PTSDepolymerization of actin filaments in sterociliaSwelling of stria vascularis, nerve endings, supporting cells- necrosis
Diagnosis—clinical• Tinnitus is the usual initial symptom with or without hearing impairment• PTA-High tone hearing loss with a notch centered on 4 kHz
Noise induced hearing Loss (NIHL)
Treatment• “Prevention is better than cure”• Awareness/Legal provisions• Reduction of noise level at place of work• Use of hearing protection devicesIntensity->85 dB, Duration- >8 hours per day 5 days a week
Idiopathic Sudden Sensori-neural Hearing Loss
Definition:30 dB or more sensori-neural hearing loss at least in 3 consecutive frequencies occurring in less than 3 days• Medical emergency• Diagnosis by exclusion of other causes on the basis of history, clinical examination,, investigations and MRI
Causes- Postulated• Viral, vascular, haematological, membrane rupture, autoimmune etc.
Idiopathic Sudden Sensori-neural Hearing Loss
Treatment- many agents, no single agent universally popular
• TUTH-Hydrocotisone IV in high doses gradually tapered over two weeks
Idiopathic Sudden Sensori-neural Hearing Loss
Prognosis- Spontaneous remission common in about 75%• Complete recovery-hearing within < 10 dB • Partial recovery-hearing within 50 % or more of prehearing• No recovery-less than 50 percent recovery
Non -Organic Hearing Loss (NOHL)
• Hysterical or malingnering- recruits or prisoners
• Disproportionate and inconsistent hearing test results
• Stenger tuning fork test• Confirmed by stapedial reflex and evoked response audiometry
Trauma to Inner Ear
• Fracture of temporal boneTransverse-U/L Severe sudden SNHL