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Ent seminar
- 1. ENT SEMINAR BY, AKASH BM III/I MBBS BELAGAVI INSTITUTE OF MEDICAL SCIENCE
- 2. PRESBYCUSIS
- 4. PRESBYCUSIS SNHL ASSOCIATED WITH PHYSIOLOGICAL AGEING PROCESS IN THE EAR Manifests at the age of 65yrs If early, * hereditary predisposition * chronic noise exposure * generalised vascular disease
- 7. PATHOLOGICAL TYPES MECHANICAL/ COCHLEAR CONDUCTIVE PRESBYCUSIS * basilar membrane stiffening * audiogram is sloping type SENSORY PRESBYCUSIS Degeneration of organ of corti Hair cell atrophy seen basal coil progress apex affects higher frequency
- 8. NEURAL PRESBYCUSIS *ITS MOST COMMON * Degeneration of cells of spiral ganglion Basal coil apex NOTE: speech discrimination is poor STRIAL OR METABOLIC PRESBYCUSIS Atrophy of stria vascularies physical + chemical process of energy production affected NOTE : Audiogram is flat but speech discrimination is good
- 10. diagnosis Audiogram (PTA) SHOWS B/L Progressive SNHL HIGH FREQUENCY PTA SHOWS Downsloping audiogram TREATMENT HEARING AIDS COCHLEAR IMPLANTS
- 13. THE DEAF CHILD Children with profound 90 db loss or total deafness fail to develop speech termed deaf mute/ deaf and dumb Aetiology * Birth (prenatal) * During birth ( perinatal) * postnatal
- 14. Prenatal causes They may pertain to the infant 0r mother INFANT FACTORS GENETIC INFANT FACTORS-----inner ear anomalies NON GENETIC ANOMALIES - NONSYNDROMIC and SYNDROMIC
- 15. ANOMALIES SCHEIBE DYSPLASIA IT ismost common inner ear anomaly bony labyrinth is normal superior part of membranous labyrinth is normal dysplasia of saccule and cochlea = cochleosacular dysplasia AR non syndromic trait
- 16. ALEXANDER DYSPLASIA It affects only the basal turn of membranous cochlea High frequencies are affected Residual hearing is + in low frequencies Can be exploited by amplification with hearing aids
- 17. BING SIEBENMANN DYSPLASIA COMPLETE ABSENCE OF MEMBRANOUS LABYRINTH
- 18. MICHEL DYSPLAIA Complete absence of bony and membranous labyrinth Petrous apex is absent but external and middle ear may be completely unaffected No hearing aids or cochlear implantation can be used
- 19. MONDINI DYSPLASIA ONLY basal coil is present or cochlea is 1.5 turn Incomplete partition between the scalae due to absence of osseous spiral lamina u/L or B/L This deformity seen in pendred Waardenburg branchio oto renal treacher Collins
- 20. ENLARGED VESTIBULAR AQUEDUCT Vestibular aqueduct is enlarged >2mm Endolymphatic sacalso enlarged Can be seen on t2 MRI It causes early onset snhl --progressive Vertigo may be present Perilymphatic fistula may occur
- 21. Semicircular CANAL MALFORMATION BOTH SUPERIOR and lateral Only lateral semi-circular canal Identified on imaging techniques
- 22. MATERNAL FACTORS Infections during pregnancy Drugs during pregnancy Radiation to mother in 1st trimester Other factors --- nutritional deficiency ,DM, toxaemia, thyroid deficiency,maternal alcoholism
- 23. Perinatal causes They relate to cause during birth or in early neonatal period 1. anoxia 2. LBW AND PREMATURITY Birth injuries Neonatal jaundice bilirubin level >20mg% Neonatal meningitis Sepsis Ototoxic drugs
- 24. POSTNATAL CAUSES 1.GENETIC 2. NON GENETIC; VIRAL INFECTIONS MENINGITIS AND ENCEPHALITIS SCRETORY OM OTOTOXIC DRUGS TRAUMA NI DEAFNESS
- 25. EVALUATION OF A DEAF CHILD FINDING THE CAUSE; -----detailed history Suspician of hearing loss the child sleeps through loud noises unperturbed Fails to develop speech at 1-2 yrs Poor performance in school
- 26. Risk factors for HL in children Family history of HL Prenatal infection TORCH Craniofacial anomalies LBW Hyperbilrubinaemia Ototoxic medications Bacterial meningitis APGAR SCORE 0-4 @1min 0-6@5min
- 27. ASSESSMENT OF HEARING IN INFANTS
- 37. 0BJECTIVE TESTS A] evoked response audiometry 1. electrocochleography 2. ABR B] OAE C] IMPENDANCE AUDIOMETRY
- 38. MANAGEMENT
- 49. THANK YOU