Downloaded 13 times
Uploaded byDr Harjitpal Singh
NONSUPPURATIVE OTITIS MEDIA
This document discusses nonsuppurative otitis media, specifically otitis media with effusion (OME). It describes the types and symptoms of OME, as well as the theories behind its pathophysiology including Eustachian tube dysfunction and reflux. Diagnosis involves history, otoscopy, tympanometry and audiometry. Treatment includes medical management with antibiotics, decongestants or antiallergics as well as surgical interventions like myringotomy, ventilation tubes or mastoidectomy.
In this document
Powered by AI
Introduction to Non-Suppurative Otitis Media by Dr. Harjitpal Singh, outlining the title and author's credentials.
Different types include Serous Otitis Media, Chronic Adhesive Otitis Media, Aero-otitis Media, and Tubercular Otitis Media.
OME, also known as Glue Ear, characterized by non-purulent effusion, can be mucoid or serous.
OME occurs often post-acute otitis media; 45% persist for 1 month; affects 3-4% of ENT patients.
Discussion on Eustachian dysfunction, reflux, gene regulation, and oxidative stress theories of OME.
Identifies bacterial flora involved and various factors leading to OME including age and dietary influences.Age-related development of the Eustachian tube and its implications for ventilation in infants.
Explains how craniofacial abnormalities, diet, racial differences, and seasonal variations affect OME.
Factors such as bottle feeding, siblings with otitis media, attendance at daycare, and socioeconomic status.
Describes the makeup of fluids within the middle ear during OME episodes.
Symptoms of OME, including hearing loss, behavioral changes, and signs of URI.
Diagnostic methods for OME involve history, otoscopy, tympanometry, and audiometric evaluation.Various otoscopic appearances in OME, tympanometric findings, and necessity for audiometry.
Overview of medical and surgical management options, including medications and procedures.
Details on ventilation tubes' function, insertion techniques, and their benefits for hearing.
Evidence showing hearing improvements post-ventilation tube insertion over time.
Potential complications associated with ventilation tubes, including dislodgement and infection rates.
Details on adenoidectomy procedure, techniques, and its role alongside ventilation tubes.
Discusses possible long-term effects of OME including necrosis, tympanosclerosis, and SNHL.
Importance of follow-up examinations in children to monitor and treat persistent OME.
Describes chronic adhesive otitis media, its causes, clinical features, and treatment options.
Aero-otitis media due to eustachian tube dysfunction, its clinical features, treatment, and prevention strategies.
Describes tuberculous otitis media symptoms, diagnosis, local treatment strategy, and necessary surgeries.
Thanking the audience for their attention.
More Related Content
Similar to NONSUPPURATIVE OTITIS MEDIA
More from Dr Harjitpal Singh
NONSUPPURATIVE OTITIS MEDIA
- 1. NONSUPPURATIVE OTITIS MEDIA Dr HarjitpalSingh Assistant Professor(ENT), Dr RKGMC, Hamirpur
- 2. NONSUPPURATIVE OTITIS MEDIA VariousTypes: Serous Otitis Media/ Otitis Media with Effusion Chronic Adhesive Otitis Media Aero-otitis Media Tubercular Otitis media
- 3. Otitis Media withEffusion (OME) Synonyms • Glue ear • Serous otitis media • Chronic nonpurulent otitis media • Silent otitis media,
- 4. Otitis Media withEffusion (OME) • Politzer described this condition in 1869 • Otitis media with effusion (OME) is characterized by a nonpurulent effusion of the middle ear that may be either mucoid or serous • Serous otitis media is a specific type of otitis media with effusion caused by transudate formation due to rapid decrease in middle ear pressure relative to the atmospheric pressure. • The fluid in this case is watery and clear. • The term glue ear has been used when there occurs a collection of thick mucus like a glue in the middle ear
- 5. • Otitis mediawith effusion (OME) can occur during the resolution of acute otitis media (AOM) once the acute inflammation has resolved. • Among children who have had an episode of acute otitis media, as many as 45% have persistent effusion after 1 month • but this number decreases to 10% after 3 months • Incidence of this disease is 3 to 4 percent of ENT disease and about 10 percent in preschool and school going children. • Remember in secretory otitis media there is no perforation in TM, which is a feature of chronic suppurative otitis media (CSOM).
- 6. PATHOPHYSIOLOGY OF OME •Eustachian dysfunction theory • Reflux theory • Gene regulation theory • Oxidative stress theory
- 7. ET DYSFUNCTION THEORY EThas 3 main functions: • Equilibration of pressure between the middle and external ears, • Clearance of secretions • Protection of the middle ear
- 8. • If ETdysfunction is persistent, • A negative pressure sets in middle ear due to diffusion of N2 and O2 into the middle ear mucosal cells • If it persists it elicits a transudate from the mucosa, causing serous effusion.
- 9. REFLUX THEORY • Presenceof reflux proven by radiography • Presence of pepsin A in the middle ear
- 10. GENE REGULATION THEORY •Upregulation of mucin genes secondary to bacterial antigen challenge. • Production of a mucin-rich effusion
- 11. OXIDATIVE STRESS THEORY •Significant changes in oxidative stress in patients with otitis media with effusion • Significantly improved but not normalized level of oxidants following the placement of ventilation tubes. • However, the role of antioxidants in the treatment of OME has yet to be fully investigated.
- 12. ETIOLOGY AND PREDISPOSING FACTORSFOR OME • The same flora found in ASOM can be isolated in OME • In OME the inflammatory process is less and volume of bacteria is less S pneumoniae is found in 35% H influenzae is found in 20% M catarrhalis is found in 4-13% Streptococcus pyogenes, Staphylococcus aureus, gramnegative enteric bacteria, and anaerobes. Pseudomonas species predominate.( long standing)
- 13. PREDISPOSING FACTORS • Infections •Age • Eustachian tube dysfunction • Craniofacial abnormalities • Diet • Racial and sex differences • Seasonal variations • Others
- 14. AGE • In infants,the eustachian tube has a nearly horizontal orientation • Develops the 45° angle (as in adults) after several years. • Size and shape of the eustachian tube at birth, unlike adults, are unfavourable for ventilation
- 16. ET DYSFUNCTION • Respiratorytract has ciliated, pseudostratified columnar epithelium • Extends up to ET and anterior part of the middle ear • Along with goblet cells they produce mucus • In OME inflammation of this epithelium in the Eustachian tube and hypotympanum. • Flat cuboidal middle ear and mastoid mucosa is patchily • The ciliary lining would appear to be less efficient • The submucosa is edematous and inflamed with dilated blood vessels and an increased number of Macrophages Plasma cells Lymphocytes
- 17. CRANIOFACIAL ABNORMALITIES • Cleftpalate (even if repaired) have deficient palatine muscles and resultant poor ET function • Down syndrome • Turner syndrome more likely to have OME, • Bifid uvula do not appear to have a higher incidence of OME
- 19. DIET • High-fat dietproven risk factor
- 20. RACIAL AND SEXDIFFERENCE • OME is higher in Native Americans • NO difference in prevalence rates between white and black populations exists. • Males may have a slightly higher preponderence (not statistically significant)
- 21. EFFECT OF SEASONALVARIATION • Twice an amount of children were diagnosed in winter with OME when compared with summer. • Probable reason could be due to increased URTIs in winter
- 22. OTHER PREDISPOSING FACTORS •Bottle feeding • Feeding while supine • Having a sibling with otitis media • Attending day care • Having allergies to common environmental entities • Having a lower socioeconomic status • Living in a home in which people smoke • Having a parental history of otitis media with effusion.
- 24. Composition of fluid Fluidin middle ear: Mixture of epithelial cells, goblet cells, mucous glands along with inflammatory exudate/ transudate intercellular spaces from the inflamed submucosa
- 25. CLINICAL FEATURES • Quiescentphase – 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.
- 26. DIAGNOSIS • History • Otoscopy •Tympanometry • Pure tone audiometry • Myringotomy and aspiration of fluid (Gold standard)
- 27. 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
- 28. Examination Tympanic Membrane –otoscopy Nasopharynx / nose –especially in adults Adequate examination of the head and neck Audiological evaluation- Tuning Fork Tests - show conductive hearing loss Tympanometry PTA Radiology Mastoids: X-ray mastoid shows clouding of air cells Adenoids: Hypertrophy seen mostly
- 29. OTOSCOPY • Unfortunately theotoscopic appearances of OME are extremely varied. • The otoscopic findings in OME are mainly different combinations of retraction of the pars tensa and variations in its color. • Retractions may be evident by indrawing of the handle of the malleus
- 31. OTOSCOPY(cont.) Appearance of TM: Color Middle Ear Yellow Fluid levels Blue Air bubbles Position Retracted Full Mobility Reduced
- 33.
- 34.
- 35.
- 37.
- 38. Left Tympanic Membranein Otitis Media with Effusion showing Bluish Discoloration
- 39. OTHER FEATURES • Tonsillarhypertrophy • Adenoid hypertrophy • Turbinate bogginess • Postnasal drip, • Rhinorrhea • Watery or erythematous eyes consistent with a concurrent URTI or environmental allergies
- 40. TYMPANOMETRY Type B tympanogramwith reduced compliance and a shift to negative side, is most of the times associated with OME Type A is infrequently associated with OME T type C falls in between
- 41. AUDIOMETRY • Audiometry ismandatory in all children with a suspected hearing impairment • Irrespective as to whether OME is diagnosed at the time. • Routine audiometric testing of the hearing of every child with OME seen at secondary care is recommended • Hearing impairment can vary enormously. • Pure tone average (PTA) shows 25 to 40 dB conductive loss and sometimes sensorineural hearing loss (SNHL) due to fluid pressing over round window. This disappears with evacuation of fluid.
- 42. COMPREHENSIVE ASSESMENT OF CHILD Needsto be skillfully done with the assistance of • ENT Surgeon • Audiologist • Pediatrician • Pediatric psychiatrist/psychologist • Nursing staff/personel trained in developmental pediatrics
- 43.
- 44. Medical Management Speed upthe resolution Antibiotics Benefits in first two weeks Long term (>6 weeks) - not recommended Nasal Decongestants Decongestants, i.e. oral decongestants and nasal decongestants in the form of drops or sprays. Antiallergics play an importantrole, especially if the cause is allergy Middle ear aeration is promoted by Valsalva, politzerization, catheterization and chewing gum exercises also help in opening the tube.
- 45. Surgical Management Myringotomy andAspiration of Fluid. Ventilation Tubes Insertion Tympanotomy or Cortical Mastoidectomy. It is sometimes required for removal of loculated thick fluid or other associated pathology such as cholesterol granuloma. Surgical Treatment of Causative Factor: Adenoidectomy, tonsillectomy, polypectomy. septoplasty or FESS or wash-out of maxillary antra may be required. This is usually done at the time of myringotomy.
- 46. MYRINGOTOMY and ASPIRATIONof FLUID • An incision is made in tympanic membrane and fluid aspirated with suction. • Thick mucus may require installation of saline or a mucolytic agent like chymotrypsin solution to liquefy mucus before it can be aspirated. • Sometimes, two incisions are made in the tympanic membrane, one in the anteroinferior and the other in the anterosuperior quadrant to aspirate thick, glue-like secretions on “beer-can” principle.
- 47. VENTILATION TUBES Synonyms Myringotomy tube, Tympanostomytube Pressure equalization (PE) tube. Introduced in 1954 by Armstrong Pressure equalization tubes (grommets)are available in a variety of sizes, shapes,
- 48. VENTILATION TUBES • Teflon,silicone, titanium, gold and be coated with materials such as silver oxide. • Permit ventilation of the middle ear and mastoid system. • Prolonged aeration of the middle ear has been shown to reverse the mucosal hyperplasia and metaplasia that accompany otitis media with effusion. • Ventilation tubes are classified as short, or long term. • Data are lacking on 'duration of tube function' • Relied upon less relevant 'duration till extrusion • Self extrude from 6 to 12 months
- 50. Ventilation Tubes Insertion •(A) Incision in ASOM; • B) (i) Curvilinear incision, (ii) Radial incision in secretory otitis media, (iii) Radial incision with grommet in place; • (C) Magnified view of a grommet
- 51. Ventilation Tubes Insertion Posterosuperiorinsertion is not recommended –damages the Ossicular Chain No difference in radial or circumferential inscion or anterosuperior and anteroinferior position. To maximize the duration-insertion in anteroinferior is recommended . Topical preparations are used to prevent tube block with blood or infection.
- 53. HEARING FOLLOWING VTINSERTION • Ventilation tubes alone will improve the hearing level by 9dB at 6 months, 6dB at 12 months 4 dB at 24 months. (persistent decrease in improvement is due to non functioning VT over a period of time) • Children randomized to have VT had a marked improvement three months following surgery of 12 Db compared with the nonsurgical group. • The younger children at day care those with binaural hearing thresholds poorer than 25 dB HL and persistent over at least 12 weeks will benefit most
- 54. COMPLICATIONS OF VTTUBE Dislodgement Blockage ( 9% without antibiotics and 1% with antibiotics) Otorrohoea Acute otorrhoea 9% Recurrent otorhoea 7% Chronic otorrhoea 3% Perforation Short term incidence 2% Long term incidence 17%
- 55. ADENOIDECTOMY • Mechanism ofaction in resolving is unclear (? source of infection ?? Physical obstruction to ET ) • Prior to VT Adenoidectomy alone was the surgical management for many years • Metanalysis showed overall effect at 6 months on the hearing of adenoidectomy was 8 dB and 12 dB for VT. • Current practice is to do adenoidectomy as an adjunct to VT
- 56. ADENOIDECTOMY TECHNIQUES Blind curettage. (risk of bleeding) Suction diathermy ablation (less risk) Selective removal of adenoid tissue and avoiding palatopharyngeal incompetence by leaving an inferior pad of tissue. (preferred) Microdebriders have also been advocated as allowing more selective removal of tissue.
- 57. SEQUELAE OF OME 1.Atrophic Tympanic Membrane and Atelectasis of The Middle Ear. In prolonged effusions, there is dissolution of fibrous layer of tympanic membrane. It becomes thin and atrophic and retracts into the middle ear. 2. Ossicular Necrosis. Most commonly, long process of incus gets necrosed. Sometimes, stapes superstructure also gets necrosed. This increases the conductive hearing loss to more than 50 dB. 3. Tympanosclerosis. Hyalinized collagen with chalky deposits may be seen in tympanic membrane, around the ossicles or their joints, leading to their fixation. 4. Retraction Pockets and Cholesteatoma. Thin atrophic part of pars tensa may get invaginated to form retraction pockets or cholesteatoma. Similar pockets may be seen in the attic region. 5. Cholesterol Granuloma. This is due to stasis of secretions in middle ear and mastoid. 6. SNHL
- 58. 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
- 59. CHRONIC ADHESIVE OTITISMEDIA • Also called fibrotic otitis media and is a condition in which adhesions have developed as a result of previous inflammation • For this condition to develop, it is necessary that a fibrinous exudate must form and stay in the middle ear for a sufficient long time • Pathological changes occur both in the middle ear mucosa and the tympanic membrane. • Adhesions develop by way of organisation of the inflammatory exudate and connective tissue proliferation from the inflamed mucosa. • The mobility of the ossicles and the membrane is diminished and ankylosis of the ossicles may occur. • Most otologists believe adhesive otitis media is a complication of inadequately treated acute otitis media.
- 60. CHRONIC ADHESIVE OTITISMEDIA • Atelectatic ear: It is a dry ear with complete collapse of thin TM towards middle ear with loss of middle ear space usually seen in advanced adhesive otitis media of grade IV type. • Grades of atelectasis: Grade I: Pars tensa is retracted medially but is not touching the incudostapedial joint. Grade II: Pars tensa retracted and is overlying the incudostapedial joint. Grade III: Pars tensa lies over the promontory without adhering to it. Grade IV: Pars tensa adheres to the promontory. Grade V: Pars tensa perforates and squamous epithelium drapes the promontory
- 61. CHRONIC ADHESIVE OTITISMEDIA Clinical Features Symptoms: • Deafness of conductive type • Long history of discharge from ear or allergy/sinusitis. Signs: • Tympanic membrane is thin and atrophic and may show middle ear structures • Mobility of TM is markedly restricted because of numerous adhesions between TM and promontory or ossicles • Calcified patches may be seen on TM.
- 62. CHRONIC ADHESIVE OTITISMEDIA Treatment • If adequate hearing is present, no treatment. • If hearing loss is of moderate degree, hearing aid is the best treatment. • Results of fenestration are poor and may result in Tullio, phenomenon, i.e. in the presence of mobile stapes, making an additional window in horizontal semicircular canal (HSCC) may give rise to vertigo in the presence of loud sounds. • Exploratory tympanotomy: It is done to find out the exact nature of adhesions but should be avoided if TM is thin and malleus and incus are fixed. • Silastic sheet may be inserted to prevent reformation of adhesions. • Use of polyethylene tubes to ventilate the middle ear through anterosuperior quadrant may help in early cases.
- 63. AERO-OTITIS MEDIA/Otitic Barotrauma •Otitic barotrauma occurs due the dysfunction of eustachian tube resulting in inability to maintain the middle ear pressure. • Usual cause is when one is traveling in an aeroplane while rapid descent is taking place or when one is doing under water diving or during compression in pressure chambers. • How it Occurs: When there occurs a difference of 90 mm Hg between the middle ear and outside, eustachian tube gets locked and sudden negative pressure in the middle earleads to retraction of TM; hyperemia and engorgement of blood vessels and transudation. Rupture of labyrinth if takes place may lead to vertigo and SNHL.
- 64. AERO-OTITIS MEDIA/Otitic Barotrauma •Clinical Features: Severe earache, deafness, tinnitus, vertigo, TM is retracted, congested, there may be effusion in middle ear Conductive type of hearing loss. • Treatment: Middle ear ventilation should be restored by decongestants, catheterization or even myringotomy. Use of vasoconstrictor and decongestants should be done.
- 65. AERO-OTITIS MEDIA/Otitic Barotrauma PREVENTION: Aero-otitiscan be prevented by the following measures: 1. Avoid air travel in the presence of upper respiratory infection or allergy. 2. Swallow repeatedly during descent. Sucking sweets or chewing gum is useful. 3. Do not permit sleep during descent as number of swallows normally decrease during sleep. 4. Autoinflation of the tube by Valsalva should be performed intermittently during descent. 5. Use vasoconstrictor nasal spray and a tablet of antihistaminic and systemic decongestant, half an hour before descent in persons with previous history of this episode. In recurrent barotrauma, attention should be paid to nasal polyps, septal deviation, nasal allergy and chronic sinus infections.
- 66. TUBERCULOUS OTITIS MEDIA •Tuberculous otitis media is usually seen secondary to pulmonary tuberculosis when the tubercle bacilli find their way through eustachian tube and rarely it may be blood borne. In this condition, small multiple tubercles may be seen in the middle ear, which may show caseation. Multiple perforations of the TM, which may join to form a big perforation is the characteristic of tuberculous otitis media • Multiple perforations seen in tubercular otitis media are due to multiple tubercles with painless yellow granulations in the middle ear, which show caseation. • Painless yellow granulation tissue not responding to usual treatment and biopsy or microscopical demonstration of acid-fast bacillus (AFB) confirms the diagnosis. • Multiple perforations may be seen in tuberculous otitis media, fungal infection, trauma due to foreign body or iatrogenic.
- 67. TUBERCULOUS OTITIS MEDIA •TREATMENT 1. Systemic Antitubercular Therapy. As being carried for primary disease. 2. Local Treatment. In the form of aural toilet and control of secondary pyogenic infection. 3. Mastoid Surgery. It is indicated for complications. Healing is delayed in tuberculous cases. Wound breakdown and fistula formation are common. Reconstructive surgery of middle ear is delayed till antitubercular therapy has been completed.
- 68.