Diseases of the Ear.pptx
- 1. Diseases of the outer ear
- 2. Cerumen impaction. • The most common cause of CHL in adults. • Risk factor: – narrow canal – hearing aid – osteoma. • Sym: Hearing loss, tinnitus and fullness. • Treatment: -Ceruminolytics drops -Manual removal -Syringing
- 3. • Indication for syringing: – if pain or hearing loss • C/I for syringing: : – TM perforation – the only hearing ear & – previous ear surgery. • Complications of syringing: – Otitis externa – Failure & – TM perforation
- 4. Otitis externa • It is a spectrum of infection of skin of the EAC. • Prevalence is estimated to be 0.4% per year. • Etiology: – disturbance of acid/lipid layer. – P.aeurginosa, p.mirabilis and s.aures are the commonest bacteria. • Predisposing factors: – associated with swimming ("swimmer's ear") – mechanical cleaning – skin dermatitides – aggressive scratching – devices that occlude the ear canal: hearing aids, headphones, etc. • Secondary bacterial infection is the major feature of otitis externa.
- 5. Staging • Pro inflammatory stage: itching and fullness. • Acute inflammatory stage: – Stages: mild, moderate or severe – Sym: Pain, itching, discharge and fullness. • Chronic inflammatory stage: – itching is the predominant symptom.
- 6. Diagnosis • The diagnosis of otitis externa is clinical. • Four major symptoms: pain, itching, discharge and fullness. • P/E: edema, erythema, tenderness, scaling and thickened canal wall skin.
- 7. Management options • Aural toilet for all stage. • Topical medications: antibiotic + steroid drops • Systemic antibiotics: if severe or complication exist. • Analgesics: for moderate and severe stage. • Prevention-
- 8. Complications • Cellulitis • Perichondritis/ Chondritis. • Chronic non resolving infection • Parotitis
- 9. Necrotizing otitis externa • It is a progressive, potentially lethal infection of the EAC, surrounding tissue and skull base. • Risk factors: – DM, elderly and immuno compromised patients. • Almost always due to p.aeurginosa and rarely aspergilus. • Pathophysiology-
- 10. Clinical manifestation • Severe otalgia- • Purulent otorrea- • Granulation tissue and edema of EAC- • Facial nerve palsy-
- 11. Diagnosis • Four important features for the diagnosis- -Persistent severe otalgia > 1month -Persistent purulent otorhea for months. -DM,immunocompromised or elderly. -Cranial neuropathy.
- 12. Management • Daily aural toilet • Antibiotics- for at least 6 weeks • Hyper baric oxygen- • Surgery- in refractory cases.
- 13. Otomycosis • Accounts for 10% of all otitis externa. • Affects 10% of the population. • Prolonged topical antibiotic treatment is the most important risk factor. • Aspergilus(80-90%) and candida(10-20%).
- 14. • Itching is the predominant symptom. • The most common finding is black, grey, green, yellow or white discharge with debris • Fungal hyphae-
- 16. Management • Aural toilet-BORRIC ACID. • Topical antifungal drops- clotrimazole ear drops. • Systemic antifungal therapy-if invasive.
- 17. Osteoma • Osteoma and exostosis are clinically and histologically distinct. • Osteomata are solitary pedunculated osseous lesions that are smooth and round arising from bony EAC. • Middle aged and women are commonly affected. • Etiology is unknown. • Mostly asymptomatic. • Treatment is indicated for symptomatic cases.
- 18. Osteoma.
- 19. Exostoses • Exostoses are broad-based osseous lesions. • They occur as multiple lesions and are often bilateral. • Exostoses are far more common in males. • It is due to cold water exposure. • Most patients are asymptomatic. • Surgery for symptomatic cases.
- 20. Exostoses
- 21. Diseases of the middle ear
- 22. Acute OM • It is an acute inflammation of the middle ear. • Commenest age group is b/n 18mon and 6yrs • Etiology: – S.pneumonia, H.inf. and M.catarrhalis. • Recurrent AOM: SUSPECT IMMUNE DEFICENCY. *Recurrent AOM: 3 episoides /6mon or 4 episoides/ year
- 23. Predisposing factors • ET obstruction or dysfunction- • Defect in mucociliary clearance- • Immuno deficiency state-
- 24. Clinical manifestation • Fever, otalgia and decreased hearing. • Ear discharge if TM is perforated. • Otoscopy: deep erythematous and bulged TM. • MX -A 10 day course of amoxicillin. -Analgesic and antipyretics. -Myringotomy -Watch full waiting-????
- 25. AOM.
- 26. Complications • Intra-temporal - Mastoiditis - Facial nerve palsy - Petrositis - Suppurative labyrinthitis • Intra-cranial - Meningitis - Epidural and subdural abscess - Brain abscess - Inflammatory sinus thrombosis
- 27. OME • It is an accumulation of serous fluid in the middle ear. • RFs: RFs to AOM. • Commenest cause of CHL in children. • CFs: Hearing loss, pain and sensation of fullness. • Otoscopy - dull immobile bulged TM. - Retracted TM - Air fluid level • Tympanogram –flat (type B).
- 29. Management • Identification and treatment of the underlying cause is important. • Conservative treatment for 3 months. • Surgery if the conservative option fails- -Grommet insertion
- 30. Chronic Suppurative Otitis Media Is a chronic inflammation of the mucosa & sub mucosa of ME e discharge via perforated TM. Impact on TM & ossicles. Can be active or inactive. Staph aures and pseudomonas arguinosa are the commenest etiologic agents.
- 31. Pathogenesis of CSOM AOM e perforation & failure to heal. OME. Ventilation Tube. Traumatic perforation Polyp, granulation tissue. Pain is not a feature.
- 32. Symptoms and Signs: - Ear discharge - Decreased hearing - Perforated membrane - Granulation tissue and/ Polyp
- 33. Management 1. Non-surgical- Aural toilet Topical Abcs. Systemic Abcs. 2. Surgical measures - tympanoplasty.
- 34. Facial nerve paralysis Causes: • Bell’s palsy(50%) • Trauma(20%) • RH syndrome • Otitis media … Palsy is not Bell’s if any of the following occur • Signs of tumor/ vesicle • Temporal bone infection/trauma • Multiple CN involvement/ palsy at birth • Signs of CNS lesion • Acute infectious mononucleosis
- 35. Bell’s palsy • Rapid onset, minimal associated symptoms & spontaneous recovery • Improvement in 3 weeks in 85% of cases • The longer the delay, the greater the sequale • Recent evidences suggest it is Herpes simplex mononeuritis Treatment • Steroids • Acyclovir • Surgical decompression • Eye care
- 36. Choleasteatoma • A cyst composed of keratinizing squamous epithelium in an abnormal place (e.g. middle ear, mastoid, temporal bone) • Variants: – Congenital- – Acquired (more common)- • Generally occurs as a consequence of otitis media and chronic Eustachian tube dysfunction • Frequently associated with retraction pockets in the pars flaccida and marginal perforations of the tympanic membrane • The associated chronic inflammatory process causes progressive destruction of surrounding bony structures
- 37. Clinical Features • Symptoms: – History of otitis media (especially if unilateral), ventilation tubes, ear surgery – Progressive hearing loss (predominantly conductive although may get sensory neural hearing loss in late stage) – Otalgia, aural fullness, fever • Signs: – Retraction pocket in TM, may contain keratin debris – TM perforation – Granulation tissue, polyp visible on otoscopy – Malodorous, unilateral otorrhea
- 38. Complications • Ossicular erosion: conductive hearing loss • Facial paralysis • Meningitis • Sensorineural hearing loss from inner ear erosion • Sigmoid sinus thrombosis • Dizziness from inner ear erosion or labyrinthitis • Intracranial abscess (subdural, epidural, cerebellar) • Temporal bone infection: mastoiditis, petrositis
- 39. Investigations • Audiogram and CT scan Treatment • There is no conservative therapy for cholesteatoma • Surgical: mastoidectomy ± tympanoplasty
- 40. Otoscelerosis • Fusion of stapes footplate to oval window so that it cannot vibrate. • Otosclerosis is the second most common cause of CHL in 15 to 50 year olds (after cerumen impaction). Ethology- Autosomal dominant, variable penetrance approximately 40% Female > male, progresses during pregnancy (hormone responsive)
- 41. Clinical Features • progressive conductive hearing loss first noticed in teens and 20’s (may progress to sensorineural hearing loss if cochlea involved) • ± pulsatile tinnitus • tympanic membrane normal ± pink blush (Schwartz’s sign) associated with the neovascularization of otosclerotic bone • characteristic dip at 2,000 Hz (Cahart's notch) on audiogram Treatment- • Monitor with serial audiograms if coping with loss • hearing aid • Vitamin D, NaF • stapedectomy or stapedotomy (with laser or drill) with prosthesis is definitive treatment
- 42. GLOMUS TUMOR • Glomus bodies are part of the diffuse neuroendocrine system. • Paragangliomas of the temporal bone arise from nonchromaffin paraganglia, or glomus bodies, which are part of a diffuse neuroendocrine system. • Glomus jugulare tumors arise within the jugular fossa, and glomus tympanicum tumors arise along the course of the tympanic branch of cranial nerve IX (Jacobson nerve) and along the course of the auricular branch of cranial nerve X (Arnold nerve).
- 43. • are the most common true neoplasm of the middle ear and are considered the most common pathologic condition involving the jugular foramen • occur most frequently in whites and predominate on the left side. • Females : males = 6:1 • CFs are related to tumor extent and vascularity. • are generally slow-growing neoplasms • conductive hearing loss and pulsatile tinnitus is the most common presenting symptom
- 44. Glomus tumor
- 45. Diseases of the inner ear
- 46. Presbycusis Definition: • sensorineural hearing loss associated with aging (5th and 6th decades) • Presbycusis is the most common cause of sensorineural hearing loss. Etiology: • hair cell degeneration • age related degeneration of basilar membrane • cochlear neuron damage • ischemia of inner ear
- 47. Clinical Features: • progressive, gradual bilateral hearing loss initially at high frequencies, then middle frequencies • loss of discrimination of speech especially with background noise present – patients describe people as mumbling • Recruitment phenomenon: inability to tolerate loud sounds • tinnitus • Recruitment Phenomenon results in a large rise in sensitivity to loud noises with relatively small changes in sound intensity. Treatment: • hearing aid if patient has difficulty functioning, hearing loss > 30- 35 dB • ± lip reading, auditory training, auditory aids (doorbell and phone lights)
- 48. Sudden SNHL
Editor's Notes
- #31: Pathogenesis of CSOM: There are a number of mechanisms by which a persistent tympanic membrane perforation may develop. In most cases, CSOM occurs as a consequence of an episode of AOM with perforation, with subsequent failure of the perforation to heal. There is also an association between OME and chronic perforation. The continued presence of a middle ear effusion leads, in some cases, to degeneration of the fibrous layer of the tympanic membrane. This weakness of the tympanic membrane both predisposes to perforation and reduces the likelihood of spontaneous healing. Traumatic perforations, particularly if large, may fail to heal. There are two main mechanisms by which a chronic perforation can lead to continuous or repeated middle ear infections: (1) Bacteria can contaminate the middle ear cleft directly from the external ear because the protective physical barrier of the tympanic membrane is lost. (2) The intact tympanic membrane normally results in a middle ear "gas cushion," which helps to prevent the reflux of nasopharyngeal secretions into the middle ear via the eustachian tube. The loss of this protective mechanism results in the increased exposure of the middle ear to pathogenic bacteria from the nasopharynx. The most commonly isolated bacteria responsible for CSOM are P aeruginosa, S aureus, and the Proteus species.
- #32: Typically, a patient with CSOM presents with a history of otorrhea, which may be either intermittent or continuous, and hearing loss. The discharge is usually mucopurulent, although chronic infection of the middle ear may lead to polyp or granulation tissue formation, which can result in bloodstained otorrhea. Pain is not a usual feature of CSOM and its presence should alert the physician to the possibility of a more invasive pathology.
- #34: Systemic antibiotics tend to have a poor penetration of the middle ear and are therefore less effective than topical antibiotics.