Conductive hearing loss Causes: Congenital: - Meatal atresia -Fixation of stapes foot plate -Fixation of malleus head -Congenital cholesteatoma
Acquired causes: EAC: wax, tumour , FB, furuncle, atresia Middle ear: -Tympanic membrane perforation -Fluid in the middle ear -Mass in the middle ear - Ossicle disruption - Ossicle fixation
Management Removal of EAC obstruction Removal of fluid from middle ear Removal of mass from middle ear Stapedectomy Tympanoplasty
Sensorineural hearing loss d/t lesions to cochlea, 8 th CN or central auditory pathway Aetiology : Congenital: present at birth d/t anomalies of the inner ear Acquired: occurs later in life d/t genetic or non genetic
Congenital SNHL Causes A.prenatal - before birth B.perinatal - during birth C.postnatal - after birth
Prenatal Infant factor: Inner ear anomaly 1.Scheibe dysplasia- cochleosaccular dysplasia 2.Alexander dysplasia- basal turn of membranous cochlea 3.Bing-siebenmann dysplasia- complete absence of membranous labyrinth 4.Michel aplasia- complete absence of bony and membranous labyrinth 5.Mondini dysplasia- only basal turn is present
Prenatal 6.Enlargement of Vestibular acqueduct and endolymphatic sac. 7.Semicircular canal malformation Maternal factors : 1.TORCHES infection in pregnancy 2.Ototoxic drugs in pregnancy 3.Radiation in pregnancy 4.Nutritional deficiency, hypothyroidisim
OTOTOXICITY Sensitivity to ototoxic side effects differ for each and every individual. Ototoxic Agents: Aminoglycoside: streptomycin, gentamycin, kanamycin, amikacin , neomycin Macrolide antibiotics: Erythromycin, azithromycin, clarithromycin Other antibiotics: ampicillin, minocycline, vancomycin , rifampicin, colistin
OTOTOXICITY Permanent HL: Aminoglycoside- damage the outer hair cells Cytotoxic drugs -damage the outer hair cells Temporary HL: Antimalarial drugs-Vasoconstriction in stria vascularis and in cochlea Analgesics- damage the cochlea Loop Diuretics- damage the stria vascularis
Noise Induced HL 1.Acoustic trauma: single brief exposure to very intense sound i.e more than 140 dB will damage the organ of corti , rupture of Reisssner’s membrane and rupture of TM, disruption of ossicles – SNHL and CHL 2.Noise induced HL: chronic exposure to low intense sounds – damage the hair cells (start from basal turn and outer hair cells first)
Noise Induced HL Audiogram shows notch at 4000Hz both in air and bone conduction. Maximum safe limit of noise exposure in working place is 90dB for 8hrs, 5 days per week ( Ministry of Labour) 3.Non auditory effect of noise: -sleep disturbance, chronic fatigue, Hypertension, peptic ulcer, irritability
IMMUNE MEDIATED INNER EAR DISEASE Defined as Bilateral SNHL > 30dB at any frequency and evidence of progression in at least one ear on two serial audiograms done at less than 3 months interval Progressive bilateral SNHL Age : 40 -50 yrs 50% associated with episodic vertigo 15% associated with other autoimmune disease( SLE, RA, U Colitis)
IMMUNE MEDIATED INNER EAR DISEASE Investigations: PTA and Speech audiometry BERA and Contrast MRI Blood test: CBC, RF, ANA, C3, C4 Level
IMMUNE MEDIATED INNER EAR DISEASE Treatment: Prednisolone 1mg/kg/day for 4 weeks Maintenance :10mg/day on alternate day (or) Methotrexate 15mg/ week for 6-8 weeks. Alternative treatment: Intratympanic steroid injection Immunoglobulin inj , plasmapheresis
SUDDEN SNHL Defined as 30dB or more of SNHL over at least 3 contiguous frequencies occurring within a period of 3 days or less. Mostly unilateral. May associated with tinnitus and vertigo Aetiology : idiopathic( MCC) Age: 50-60 years Spontaneous recovery rate 32-65%
SSNHL Management: 1.Steroids: Systemic: -prednisolone 1mg/kg /day (max 60mg) for 5 days then 10mg less each day until day 10 (A dose of 60mg of prednisolone= 48mg of methylprednisolone=10mg of dexamethasone) Intratympanic steroid: 10-24mg/ml of Dexa or 30-40mg/ml of methylprednisolone 4 doses over 14 days
SSNHL 2.hyperbaric oxygen : intermittent inhalation of 100% O2 in chambers pressurized above 1 atmosphere absolute 3.dextran (LMW) 4.inhalation of carbogen : ( 95% O2 + 5% CO2) 5 salt restricted diet Prognosis: 50% of the patients will improve spontaneously within 2 weeks Poor prognosis: -age above 60, associate with vertigo, present with profound HL
PRESBYACUSIS SNHL associated with physiological ageing process in the ear is called Aka Age related sensorineural hearing loss Usually starts after 60 years It’s a diagnosis of exclusion
PRESBYACUSIS 4 Histological subtypes: 1.sensory: degeneration of hair cells and sustentacular cells at the basal end of the organ of corti - Speech Discrimination is poor 2.neural: degeneration cochlear nerve neurons and cells of spiral ganglion- SD is poor 3.Metabolic or vascular : atrophy of stria vascularis – SD is good 4.cochlear conductive – stiffening of the basilar membrane due to increased number of fibrillar layer
PRESBYACUSIS Symptoms: Difficulty in hearing conversation in a noisy surrounding( lack of clarity) Tinnitus R/o head injury, meningitis, systemic illness, previous history of ototoxic drug exposure, family history of early onset of hearing loss
PRESBYACUSIS Investigations: Pure tone audiogram -symmetrical high frequency SNHL Contrast MRI -Asymmetry SNHL ( PT Average > 10dB in 0.5, 1, 2, 4 kHz frequencies) or 20dB or more at any single frequency
PRESBYACUSIS Non-specific management Reduction of background noise Encourage face to face conversation Use wireless headphones to watch TV Lip reading classes Specific management Binaural hearing aid, cochlear implant Tinnitus retrainning therapy