This document provides information on otitis media with effusion (OME), also known as glue ear. It defines OME as the accumulation of mucus within the middle ear and mastoid air cell system for 3 months or longer. The document discusses the prevalence, histology, characteristics, microbiology, role of biofilms, predisposing factors, investigations, management options including medical treatment, surgical treatment with ventilation tubes and adenoidectomy, complications, and outcomes of OME.

1. HOD: Dr. Dhinakaran M.S
Moderator: Dr. Arul
sundaresh kumar M.S
Presentor:Dr.E.Selvapriya
MS PG
Volume II
Chapter : 13
Pages no: 115 - 131

2. DEFINITION:
• Accumulation of mucus with in the middle ear and
mastoid air cell system.
• 3 months or longer- chronic
• also known as GLUE EAR,
Serous otitis media
Secretory otitis media
• Can occur with or without history of AOM.
• May present with delayed speech, language development,
poor social behaviour and difficulties with balance.

3. PREVALANCE
 8O% of children had single episode of OME before 3 years,
40% have 3 or 4 episodes.
 Among children who had AOM ,45% have persistent
effusion after 1 month.
 Bimodal at 2 and 5 years
 first attends playgroup school
 when goes to primary school.
 Above 15 years- prevalance 0.6%.

4. HISTOLOGY:
o ET and anterior mesotympanum – ciliated pseudostratified
columnar epithelium.
o This mucosa contains goblet cells and mucus secreting
glands.
o Middle ear mucosa contains flat cuboidal epithelium.
o Inflammation of the epithelium and production of mucus
or serous effusion results in OME.
o Flat cuboidal epithelium is replaced by thicker
pseudostratified mucus secreting epithelium.

5.  Ciliary lining is less efficient at moving the
secretions in to the nasopharynx than normal.
 Goblets cells are frequently present and mucus
secreting glands are formed.
 Submucosa is edematous, inflamed with dilated
blood vessels, increased number of macrophages,
plasma cells and lymphocytes.

6. CHARACTERISTICS
 Glycoprotein mucin
 IgA
 Lysozyme
 Interleukins
 Cytokines
 Adhesiveness and poor mucociliary
transportability are characteristics of the effusions

7. MICROBIOLOGY
 Streptococcus pneumoniae
 Hemophilus influenza
 Moraxella catarrhalis
 66% of cultures were negative by traditional
culture techniques.
 In case of PCR techniques, 36% of middle ear
mucosal biopsy shows intracellular streptococcus
pneumoniae.

8. ROLE OF BIOFILMS
• Biofilms – communities of sessile bacteria, resistant to
disruption, low metabolic rate.
• They are embedded in matrix of extracellular polymeric
substances and adhere to a foreign body or mucosal
surface.
• Biofilms demonstrated in 92% of middle ear mucosal
specimens of patients undergoing ventilation tube
surgery.
• High grade biofilm formation is also found on adenoid
samples – aetiology of OME.

9. PREDISPOSING FACTORS
 URI
 Age
 Allergy
 GERD
 ET dysfunction
 Craniofacial abnormalities
 Genetic factors
 Racial and sex differences
 Seasonal variations

10. AGE:
 In infants, Eustachian Tube – nearly in horizontal
orientation.
 Develops 45 degree angle after several years.
 This orientation is highly unfavourable for
ventilation.

11. ALLERGY
• There is conflicting evidence on the importance of
atopy and allergy in pathogenesis of OME.
• Among the children with history of OME, 89% had
e/o allergic rhinitis, 36% had asthma and 24% eczema
which implies allergy.
• Nasal smears and skin prick testing, with blood
eosinophil count and total immunoglobulin IgE could
be done.
• Children with OME with a family history of allergy
most likely to have a positive finding of Rhinovirus in
the middle ear cavity.

12. GERD
 During swallowing, fluid can travel from the
nasopharynx via the eustachian tube in to the middle
ear.
 Common in two thirds of infants at 4 months of age.
 Pepsin was identified in middle ear fluid in children
with OME.
 Mucosal damage can be mediated by proteolytic
activity of pepsin.
 Helicobacter pylori confirmed by PCR in middle ear
effusions.

13. ET DYSFUNCTION
ET has 3 main functions:
• Equalisation of pressure
• Clearance of secretions
• Protection of middle ear
In case of persistent ET dysfunction,
• Defective aeration of middle ear
• Negative pressure sets in
• Transudation from mucosa– effusion.

15. GENE REGULATION THEORY
URI, AOM, infection of adenoid
Release of inflammatory mediators
Upregulation of mucin genes
Effusion of increased mucus from the glands

16. CRANIOFACIAL ABNORMALITIES
 Cleft palate and even if repaired – defective
palatine muscles and resultant poor ET function.
 Downs syndrome
 Turner’s syndrome
 Bifid uvula do not appear to have a higher
incidence of OME.
 Subtotal removal should be performed under
direct vision to reduce the higher risk of
velopharyngeal insufficiency.

17. GENETIC FACTORS
In children who had OME during the first 2
years of life, there was a greater concordance in
monozygotic twins than dizygotic sets.
RACIAL AND SEX DIFFERENCES
 No difference in prevalance rates between White
and Black population
 Males have a slightly higher prepondarance
(statistically not significant)

18. SEASONAL VARIATIONS
 Twice an amount of children – winter > summer
 Propable reason - increased frequency of URIs
and ear infections.
 Due to close house hold contacts.

19. DURATION AND RECURRENCE OF EPISODES
 Median duration of effusions was 3 months.
 Infants were twice as likely to develop unilateral as
opposed to bilateral OME.
 After one month, in infants with a unilateral effusion,
50% had resolved
20% had become bilateral
30% remained unilateral.

20. RISK FACTORS FOR PERSISTENCE
 In primary care, whether a child had frequent or upper
respiratory symptoms at the time of assessment is an
important determinant for persistence of OME.
 In secondary care, the degree of associated hearing
impairment predicts persistence.
 The only modifiable risk factor is maternal smoking.

21. OTHERS
 Bottle feeding
 Having sibling with otitis media
 Attending day care
 Lower socioeconomic status
 Living in a home where people smoke
 Parental history of otitis media with effusion

22. HISTORY
 Ear pain
 Decreased hearing- 19.7%
 Recurrent URI
 Mouth breathing and snoring
 Poor speech and language development
 Signs of difficulties with balance
 Inattention and behaviour problems
 Difficulty taking part in group activities

23. Also important to confirm
• Normal pregnancy
• Delivery
• Neonatal period
• Neonatal hearing screening (OAE)
Because children with co morbidities are most
commonly affected by OME and is mostly
persistent.

24. EXAMINATION
 Otoscopy
 Otomicroscopy
 Pneumatic otoscopy
 Tuning fork tests
 Free field voice testing

25. OTOSCOPY
•Difficult to attempt due to uncoperative child or
else view obscured by wax. (Sodium bicarbonate and
olive oil drops to soften the wax)
Findings:
• Retraction of pars tensa
• OME fluid and bubbles-
For severe cases
• Variations in colour of TM

28. OTOMICROSCOPY
 Intraoperative oto microscopy performed by specialist
im the anesthetized child prior to myringotomy
achieves greater diagnostic accuracy – 94.1%.
PNEUMATIC OTOSCOPY:
• Primary diagnostic method for OME
• But requires greaterclinical skills to diagnose.

29. PNEUMATIC OTOSCOPY

30. TUNING FORK TESTS
• Poorly predicts conductive hearing loss in
children among 2 to 11 years.
FREE FIELD VOICE TESTING
• In children over the age of 3 years, the sensitivity
of modification of the voice test is 96% and
specificity is 98%.
• This is useful if audiometry is unavailable.

31. INVESTIGATIONS
 TYMPANOMETRY:
• Type B tympanogram is most of the times associated
with OME.
• Type A infrequently associated with OME .
• Type C falls inbetween.
• Otoscopy suggests OME with type B tympanogram-
combined sensitivity – 98%.
• When otoscopy suggests no OME with type A
tympanogram – specificity – 98%.

32. AUDIOMETRY
 Audiometry is mandatory in all children with a
suspected hearing impairment
 Irrespective of whether OME is diagnosed
 Routine audiometric testing of every child with OME
at secondary care is recommended
 Presence of air bone gap of greater
than 30 dB is necessary to predict
OME.
 OME with CHL, ass with Cahart
notch in bone conduction thresholds
around 2 kHz.

33. X RAY
 X ray nasopharynx lateral view - to rule out
adenoids.

34. COMPREHENSIVE ASSESSMENT
 Speech and language:
• Hearing impairment from OME is likely to impede
normal speech and language development.
• Speech reception in noise (SiN) is a better tool
than pure tone audiometry to predict benefit from
surgical intervention.
• Appears to be a small but significant long term
effects in sound discrimination in children with a history
of OME.

35.  Cognition- The influence of OME as one of many
interrelated variables affecting a child’s intellectual
development is difficult to determine.
 Balance – 30% of children are clumsy and
imbalanced. 61% of children have objectively
defective motor proficiency.
 Behaviour can be assessed using Questionarrie
reporting by parents or teachers.
 RUTTER SCORE – Antisocial , neurotic,
hyperactive and inattentive behaviour scores.

36. MANAGEMENT
 Wait for spontaneous recovery
 Medical
 Surgical

37. MEDICAL
• Nasal topical steroids
• Systemic steroids – are effective in short term (2
weeks) when combined with antibiotics.
• Antibiotics: no statistically significant benefit in the
short term.
In the longer term appeared to be slight benefit
from use of antibiotics.
• Nasal decongestants

38.  Mucolytics – no significant benefit.
HAVE NO SIGNIFICANT EFFECT IN
RESOLUTION OF OME ACC TO RCT AND META
ANALYSIS.
 Autoinflation: Because of low cost and absence of
reported adverse effects ,autoinflation – the most
promising non surgical management to augment
active monitoring.( Watchful waiting )
 Homeopathy: No randomized controlled trials have
been identified.

39. SURGICAL MANAGEMENT
 INCLUSION CRITERIA
•Children aged 3,5,7 years
• Bilateral OME
• Persistent over 12 weeks
• Hearing impairment of 20 dB HL/poorer
 MYRINGOTOMY AND ASPIRATION
• Without insertion of ventilation tube is
ineffective.

40. VENTILATION TUBES
 Introduced in 1954 by ARMSTRONG
 TEFLON, Silicone, Titanium, Gold and silver
oxide coated tubes.
 Ionized, processed silicone- resistant to biofilm
formation – reduces the incidence of plugging of
the tube and otorrhea.
 Short and long term tubes
 Usually self extrudes within 6 months.

41. TYPES
 A-Shephard’s Grommet
 B-Armstrong’s Grommet
 C-Donaldson’s Grommet
 D-Shah’s Grommet
 E- T Tube – LONG TERM
 Absorbable ventilation tubes
made from poly bisphosphazene.

42. SITE OF INSERTION
 Anteroinferior quadrant –reduces the incidence of
perforation.
 radial or circumferential incision – stay slonger.
 Posterosuperior insertion is not
Recommended because of
damaging of ossicular chain.

43.  Associated aspiration of middle ear fluid before
insertion of tube is not significant.
Aspiration produces some complications:
 Tympanosclerosis
 Trauma
 Bleeding
 Noise induced hearing loss
 Biofilm infection

45. HEARING OUTCOMES
• Ventilaton tubes alone improves the hearing level by
9 dB at 6 months
6 dB at 12 months
4 dB at 24 months
(decrease in improvement of hearing due to non
functioning of VT over a period of time)
• Younger children at day care and those with binaural
hearing thresholds poorer than 25 dB HL and
persistent over at least 12 weeks will benefit most.

46. ADENOIDECTOMY
 Not a definitive treatment
 Considers as a Chronic source of infection
 Chronic inflammatory changes in mucosa of ET
and middle ear secondary to biofilm infection of
adenoid rather than physical obstruction of
Eustachian tube is the likely cause and removing
this is how adenoidectomy is beneficial in the
management of OME

47. PROCEDURES
 Blind curettage - risk of bleeding, poor access to
the choanal adenoid and risk of trauma to the
eustachian tube.
 Suction diathermy (minimal loss)
 Coblation and microdebrider – direct vision
techniques.
 KTP laser- nasopharyngeal stenosis

48. HEARING OUTCOMES
 Metaanalysis – effect of hearing at 6 months was 8
dB.
 Adenoidectomy at the time of insertion of
ventilation tubes doubled the benefit and
extended hearing and reduces the need for
re insertion of VT.

49. COMPLICATIONS OF VENTILATION TUBES
 Operative:
• Displacement of the ventilation tube into the
middle ear – 0.5%.
• Posterosuperior myringotomy is avoided due to
damage of ossicular chain and incudostapedial joint.
• A high dehiscent jugular bulb may be pierced
byh inferiorly placed myringotomy.

50. Early postoperative:
 Blockage of lumen of tubes – Early infection
around 9%.
Topical antibiotic steroid drops at the time of
surgery reduces the incidence up to 1 %.
 Otorrhea in association with ventilation tube in
situ may due to upper respiratory tract infection or
due to chronic biofilm infection.
Post operative otorrhea is the most common
complication with incidence of 10 to 50 %.

51. Granulation tissue secondary to infection
occurs in approximately 1 %
Ofloxacin is the preferable topical antibiotic
than ciprofloxacin.

52. Late postoperative
 Hearing loss – myringotomy or insertion of ventilation
tubes not resulted in a significant difference in long
term hearing level
 Tympanic membrane perforation:
• Initial pars tensa perforation usually heals.
• Perforation may reoccur at the same site following
another episode of AOM – normally heals
spontaneously.

54. • Pars tensa retraction:
Thinning and retraction of the tympanic
membrane are complications of persistent OME.
In children with bilateral OME, pars tensa
retraction up to incus or promontory occurs in 8% of the
better ear and 10% of the poor hearing ears.
• Pars tensa atrophy:
• Ventilation tubes are not inserted
to prevent the occurrence of atrophy
and retraction.

55. Myringosclerosis
 The most common structural complication after
ventilation tube insertion – long term tubes.
 Hyaline degeneration of the collagen tissue in the
fibrous layer of the pars tensa is visible otoscopically as
white patches or plaques.
 Do not occur in the absence of history of otitis media.
 Frequency of myringosclerosis increases with
frequency of OME.
 No hearing impairment resulted from the presence of
myringosclerosis.

56. Myringosclerosis

57.  Swimming and water contamination:
Ear protection does not or only slightly
reduces otorrhea in children following insertion of
ventilation tubes.

58. THANK
YOU!