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05 ome
Otitis media with effusion, also known as serous otitis media or glue ear, is defined as the chronic accumulation of fluid in the middle ear caused by Eustachian tube dysfunction. It is a common reason for pediatric visits and the most frequent cause of hearing loss in children. Risk factors include young age, male gender, attendance at daycare, and winter season. Diagnosis involves tympanometry showing a flat tympanic membrane and treatment options include watchful waiting, antibiotics, myringotomy with tube insertion, or adenoidectomy. Complications can include permanent hearing loss if left untreated.
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05 ome
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- 2. • Definition • Introduction •Epidemiology • Aetio pathogenesis • Clinical presentation • Diagnosis • Treatment • Sequelae 2
- 3. Otitis media witheffusion (OME) Defined as Chronic accumulation of mucus within middle ear and sometimes mastoid air cell system. Time for fluid to be present – 12 weeks 3
- 4. Synonyms •Otitis media catarrhal •Subacute catarrh of middle ear •Mucous aural catarrh •Exudative catarrh •Adhesive catarrh •Chronic middle ear exudate catarrh •Secretory otitis media •Chronic non suppurative otitis media 4 Introduction •Serous otitis media •Otitis media with effusion •The hypersecretory ear •Tympanic hydrops •Glue ear •Otitis media ex vacuo •Exudative otitis media •Indolent otitis media •Sero mucinous otitis media •Mucoid otitis media
- 5. • $3.5 billionin expenditures in USA • Most common reason for visit to pediatrician • In the developed world AOM is the most common cause for prescribing antibiotics in children and accounts for over 90% of all antimicrobial consumption during the first 2 years of life (Dagan, 1995). • Tympanostomy tube placement is 2nd most common surgical procedure in children • Development of multidrug-resistant bacteria • Most common cause of acquired HL in pediatric age Introduction : the burden of otitis media 5
- 6. • Egyptian mummieshave perforations of TM and mastoid destruction • 450 BC: Hippocrates described the disease • 1704: Valsalva maneuver and Toynbee – ET dysfunction with negative ME pressure • 1869: Politzer described OM catarrahalis & its treatment as insufflation of air & paracentesis of middle ear • Jean Riolan: Inadvertant puncture of TM- tympanocentesis. Fell into disrepute for decades. • 20th century: Schwartz reintroduces tympanocentesis • 20th century: Armstrong – use of tympanostomy tubes • Post World war II- Nasopharyngeal radium irradiation. Given up for potential for malignancies Introduction : History of otitis media 6
- 7. Epidemiology : riskfactors I. Host-Related factors (intrinsic or genetic) • Age • Gender : males more prone to persistent OME • Race : American natives and Eskimos > whites > blacks • Cleft palate/craniofacial abnormality/Down Syndrome • genetic • Allergy (no support to prove) 7
- 8. 2. Environmental oraetiological factors (extrinsic) • season and upper respiratory infection • day care / home care • siblings • passive smoking (negligible risk.) • breast feeding / bottle feeding • socio-economic status 8
- 9. Aetio pathogenesis No singlecause for OME in children • Viral URI • Eustachian tube dysfunction • Middle ear gas composition • Nasopharyngeal disproportion 9
- 10. Developmental Differences betweenInfants and Adults in Anatomy of the Eustachian Tube* • Adults – ant 2/3- cartilaginous – post 1/3- bony – 45 degree angle – nasopharyngeal orifice 8-9 mm • Children – longer bony portion – 10 degree angle – nasopharyngeal orifice 4-5 mm in infants 10
- 11. Eustachian tube • Usuallyclosed • Opens during swallowing, yawning, and sneezing for 2 sec • Opening involves cartilaginous portion • Tensor veli palatini responsible for active tubal opening • No constrictor function 11
- 12. Role of theEustachian Tube 1. Pressure regulation of middle ear 2. Clearance ‘Drainage’ of middle ear secretions mucociliary muscular 3. Protection from sound and secretion anatomic immunologic and mucociliairy 12
- 13. Eustachian Tube Dysfunction •Palatal abnormalities • Cleft palate • Sub mucous cleft palate • Altered mucociliary system • Infection • Allergy • Immunological factors • Surfactant deficiency • Cilial abnormalities • Hormonal factors 13 Aetio pathogenesis
- 14. Aetio pathogenesis • Middleear gas composition – Acts as gas pocket – Spectrometry shows middle ear gas partial pressures • PN2 – 82.4 percent • PO2 – 7.6 percent • PCO2 – 10.0 percent – Closely resemble mixed venous blood and not atmospheric air – Theories of middle ear gas deficiency 14
- 15. Theories of middleear gas deficiencies • Hydrops ex vacuo theory • Ventilation deficiency theory • Sniff theory • Excess diffusion theory 15
- 16. Anatomic obstruction Intrinsic Inflammation Extrinsic adenoid Tumor ObstructionWeak TVP Open Functionalobstruction Ventilation deficiency theory 16
- 17. Theories of middleear gas deficiencies • Hydrops ex vacuo theory • Ventilation deficiency theory • Sniff theory • Excess diffusion theory 17
- 18. Aetio pathogenesis • Nasopharyngealdisproportion • Cranio facial abnormalities • Adenoids and nasopharynx – Mechanical blockage of ET – Focus of infection 18
- 19. Related Clinical Conditions •Barotrauma • Diving / flying / HBO therapy - OM even in normal ET function • NP tumors • Radiation therapy • Inadequate antibiotic therapy • Gross DNS • Neoplasms • Syndromic diseases 19 Aetio pathogenesis
- 20. Pathology • Normal flatcuboidal middle ear and mastoid epithelium – thickened pseudostratified mucus secreting epithelium • Goblet cells , mucus secreting glands • Ciliary lining less efficient • Defective mucociliary clearance • Submucosa – oedematous – with dilated blood vessels and increase in no. of macrophages and lymphocytes 20
- 21. Resolution of acuteinflammation and bacterial infection -- a failure of the middle ear clearance mechanism allows OME to persist. Factors implicated in the failure of the clearance mechanism: •ciliary dysfunction •mucosal edema •hyperviscosity of the effusion •possibly, an unfavorable pressure gradient. 23
- 22. Composition of fluid •Fluid in middle ear – mixture of epithelial cells, goblet cells, mucous glands alongwith inflammatory exudate/ transudate – intercellular spaces from the inflamed submucosa • Bacteria isolated in 1/3rd of cases • Biochemical: increase protein concentration. • OME: sclerotic mastoids – Children – smaller mastoids – Pneumatization less with recurrent episodes 24
- 23. Pathogenesis of OM InfectionET dysfunction Host response Liberation of inflammatory mediators Increase of vascular permeability Increase of glandular secretion Inflammation Mucosal proliferation 26
- 24. • Quiescent phase– Asymptomatic • Covert or overt hearing loss • Impaired speech and language development • Behavioral changes • Indirect symptoms of hearing loss • Otalgia – due to secondary infection • Features of associated URI, Nasal pathologies • Symptoms of palatal abnormality or syndromic conditions with cranio facial abnormalities 27 Clinical features
- 25. • History • Otoscopy •Tympanometry • Pure tone audiometry • Myringotomy and aspiration of fluid (Gold standard) 28 Diagnosis
- 26. Medical history Hearing loss Otalgia: ear pulling, irritability Otorrhoea Fever Preceding upper respiratory tract infection Purulent conjunctivitis (Haemophilus influenzae) Vertigo : not common as a complaint, unilateral disease, clumsiness Nystagmus : labyrinthitis Tinnitus Swelling about the ear : DD mastoiditis, external otitis, adenitis Facial paralysis 29
- 27. Examination • Tympanic Membrane– otoscopy • Nasopharynx / nose –especially in adults • Adequate examination of the head and neck 30
- 28. • Audiological evaluation- –TFT – Tympanometry – PTA-Conductive Loss of 10-40dB • Radiology -Mastoids -Adenoids 31 Examination
- 29. TYPE B TYMPANOGRAM:FLAT OR NO PEAK, SEEN IN OTITIS MEDIA WITH EFFUSION 32
- 30. • Audiological evaluation- –TFT – Tympanometry – PTA-Conductive Loss of 10-40dB • Myringotomy and aspiration of fluid (Gold standard) • Radiology -Mastoids -Adenoids 33 Examination
- 31. I. Counselling andhearing tactics • Parents of children of OME often misinformed-both overpessimistic and overoptimistic. • Counsel about benign nature and high spontaneous resolution rates as well as natural history of disease. • Concern about hearing – Impairement associated with OME variable and mild or moderate at most. • Minimise disability by Hearing tactics TREATMENT 34
- 32. II. Medical therapy •Antibiotic therapy - modest impact on short-term and impact on long-term resolution is smaller. • Steroid therapy and antihistamine-decongestant therapy - no proven effect • Ventilate the ET- No URTI • Valsalva • Chewing gums • Politzerization • Auto inflation using otovent balloons-older children • Mucolytic agents – no long term effect. • Management of associated nasal condition / allergy • Homeopathy – not shown to be of benefit TREATMENT 35
- 33. III. Surgical therapy •(a) Myringotomy and aspiration • (b) Ventilation tubes • (c) Adenoidectomy • (d) Rarely explorative tympanotomy with/without mastoidectomy • No improvement > 90 days of treatment • Persistent OME with hearing loss in children • Chronic effusion • Reassessment at pre admission clinic for persistence 36
- 34. (b). Myringotomy withventilation tubes • Diagnostic • OME –therapeutic • Types of ventilation tubes • Procedure – • Outcomes 37
- 35. Tympanostomy Tubes • Siliconerubber • Teflon • Plastic • Precautions-flange – Not too near the annulus 38
- 36. Tube Choice • Standardgrommets (Armstrong, Shepard, collar button) – Persistent perforation rates 3-5% – Persist 6-18 months • Goode T-tubes – Persistent perforation rates 10 of 64 in best study – Persist 2-4 yrs • Bioabsorbable/bacteriostatic grommets – New choice in future – Made of bacteriostatic polylactic acid – Similar material to resorbable miniplates – Mix can be customized to persist a given amount of time 39
- 37. Myringotomy with ventilationtubes • Diagnostic • OME –therapeutic • Types of ventilation tubes • Procedure – • Outcomes 40 • Complications -
- 38. (c). Adenoidectomy • Rationale •Recommendation • Effect on hearing improvement 41 IV. Hearing Aids
- 39. 100 90 80 70 60 50 40 30 20 10 0 0 1 23 4 5 6 7 8 9 10 Proportion(%)withfluidremaining Survival functions for time to fluid Clearance as Confirmed by otoscopy • No surgery (n=77) • Ventilation tube only (n=77) • Adenoidectomy only • Adenoidectomy and tube (n=136) Years Maw et al, 1994 42
- 40. Treatment Recurrent Otitismedia • Chemoprophylaxis – Sulfisoxazole, amoxicillin, ampicillin – less efficacy for intermittent propylaxis • Myringotomy and tube insertion – Decreased frequency and severity of AOM – otorrhoea and other complications – may require prophylaxis if severe • Adenoidectomy – 28% and 35% fewer episodes of AOM at first and second years 43
- 41. Sequelae Of OME •Scarring • Atelectasis • Attic retraction • Tympanosclerosis • Otorrhoea • Perforation • COM / cholesteatoma • SNHL • Behavioural/ developmental 44
- 42. Follow-up • Child shoulddemonstrate symptomatic benefit within 72 hours of antibiotic • Failure to show improvement - re-evaluation. • A follow-up examination - one month after the diagnosis and should include: - Inspection of the tympanic membrane - Assessment of hearing • The purpose of the follow-up - identify persistent otitis media or persistent middle ear effusion • Children with persistent otitis media or persistent middle ear effusion - seen on a monthly basis until their exam is normal 45
- 43. Future solution • Immunisationwith Haemophilus influenzae type B vaccine • Heptavalent pneumococcal conjugate vaccine PCV7 • Attempt to produce vaccine for nontypable H. influenzae and M. catarrhalis • Surfactants 46
- 44. Bibliography 47 • Scott BrownOtorhinolaryngology, Head and Neck surgery, 6th and 7th edition • Ballenger’s Otorhinolaryngology, Head and Neck surgery, 17th edition • Ludman and Wright diseases of the ear, 6th edition
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