NONSUPPURATIVE OTITIS MEDIA

1. NONSUPPURATIVE
OTITIS MEDIA
Dr Harjitpal Singh
Assistant Professor(ENT),
Dr RKGMC, Hamirpur

2. NONSUPPURATIVE OTITIS MEDIA
Various Types:
 Serous Otitis Media/ Otitis Media with Effusion
 Chronic Adhesive Otitis Media
 Aero-otitis Media
 Tubercular Otitis media

3. Otitis Media with Effusion (OME)
Synonyms
• Glue ear
• Serous otitis media
• Chronic nonpurulent otitis media
• Silent otitis media,

4. Otitis Media with Effusion (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 media with 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
ET has 3 main functions:
• Equilibration of pressure between the middle and external ears,
• Clearance of secretions
• Protection of the middle ear

8. • If ET dysfunction 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
• Presence of 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
FACTORS FOR 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
• Respiratory tract 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
• Cleft palate (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 diet proven risk factor

20. RACIAL AND SEX DIFFERENCE
• 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 SEASONAL VARIATION
• 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
Fluid in middle ear:
Mixture of epithelial cells,
goblet cells,
mucous glands
along with inflammatory exudate/ transudate
intercellular spaces from the inflamed
submucosa

25. CLINICAL FEATURES
• 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.

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 the otoscopic 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 T M:
Color Middle Ear
Yellow Fluid levels
Blue Air bubbles
Position
Retracted
Full
Mobility
Reduced

33. Retraction

34. Bubbles

35. Air Fluid Level

37. Bulging

38. Left Tympanic Membrane in Otitis Media with Effusion showing Bluish Discoloration

39. OTHER FEATURES
• Tonsillar hypertrophy
• Adenoid hypertrophy
• Turbinate bogginess
• Postnasal drip,
• Rhinorrhea
• Watery or erythematous eyes consistent with a concurrent URTI or
environmental allergies

40. TYMPANOMETRY
Type B tympanogram with 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 is mandatory 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
Needs to be skillfully done with the assistance of
• ENT Surgeon
• Audiologist
• Pediatrician
• Pediatric psychiatrist/psychologist
• Nursing staff/personel trained in developmental pediatrics

43. MANAGEMENT
• Medical
• Surgical

44. Medical Management
Speed up the 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 and Aspiration 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 ASPIRATION of 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,
Tympanostomy tube
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
Posterosuperior insertion 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 VT INSERTION
• 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 VT TUBE
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 of action 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 should demonstrate 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 OTITIS MEDIA
• 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 OTITIS MEDIA
• 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 OTITIS MEDIA
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 OTITIS MEDIA
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-otitis can 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. Thank You