inflammation of middle ear is a common disease.

1. INFLAMMATORY
CONDITIONS OF
MIDDLE EAR
PRESENTED BY
DR ANKIT K.
TIWARI
RSO ENT ,3RD YR
GMC ,BHOPAL

2. CONTENTS
 INTRODUCTION
 DIFFERENT TYPES OF ME INFECTION
- AOM
- OME
- ANOM
- COM
- GRANULOMATOUS DISEASE

3. INTRODUCTION
 Middle ear is a central part of middle ear cleft.
 Middle ear cleft is made up of – Eustachian tube, middle ear
cavity(tympanum), mastoid air cell system.
 Middle ear is an air containing cavity which is aerated by eustachian
tube.
 ME have negative air pressure d/t continuous absorption of air by ME
mucosal lining & due to swallowing movement.
 To keep ty,mpanic membrane at its normal position with its landmark
the net ther pressure difference between middle ear cavity & EAC
should be zero.

4. INTRODUCTION
 Any possible
change in this
difference can
lead to
retraction or
bulging of the
tympanic
membrane &
thus affecting
middle ear
ventilation which
can lead to
various
pathologies.

6. ACUTE OTITIS MEDIA
 It is defined as suppurative infection involving the mucosal lining of
middle ear cleft. The term acute is used to indicate infections of less
than 3 weeks duration
 Middle ear cleft includes Eustachian tube, middle ear, attic, aditus,
antrum and mastoid air cells.

7. ACUTE OTITIS MEDIA
 AETIOLOGY –
 More common especially in infants and children of lower socioeconomic group.
 The disease typically follows viral infection of upper respiratory tract:
- Rhinovirus
- RSV
- Influenza virus
- Enterovirus
 Most common organism in infants and young children are -
• Streptococcus pneumoniae -30%
• Hemophilus influenzae -20%
• Moraxella catarrhalis -12%
• Strep. pyogens, Staph. aureus, P
.aurugenosa are also involved
• No growth in about 18-20% of cases

8. ACUTE OTITIS MEDIA
 ROUTE OF INFECTION –
1. Via Eustachian tube.
 It is the most common route.
 Childrens are more susceptible.
 Eustachian tube in infants & young children is shorter, wider, more horizontal & less
stiff.
 Large adenoids can interfere with the opening of the tube.
 Immune system is not fully developed.
 A small tube connecting the middle ear to the nasopharynx.
 FUNCTIONS -
 Regulate and equalize pressure of middle ear.
 Prevent fluid from accumulating in the middle ear.
 Protect from the nasopharyngeal infection.

9. •In children ET is at an angle of 10° while in adults it is at an angle of
45°.
•ISTHMUS is a narrowing in the ET, at the junction of the
cartilaginous and bony part.
•It is only present in a
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10. ACUTE OTITIS MEDIA
2. Via External Ear:
traumatic perforations of TM d/t any cause associated with TM
perforation
 Eg. TM trauma, insertion of tympanostomy tubes, tympanometry,
myringotomy
3. Blood borne: uncommon route.

11. ACUTE OTITIS MEDIA
 PRE DISPOSING FACTOR –
• Anything that interferes with normal functioning of ET, it could be:
1. Recurrent attacks of common cold, URTI and exanthematous fevers like measles,
diphtheria or whooping cough.
2. Infections of tonsils and adenoids.
3. Chronic rhinitis and sinusitis.
4. Nasal allergy.
5. Tumors of nasopharynx, packing of nose or nasopharynx for epistaxis.
6. Cleft palate: caused by anatomic problems in the muscles that open the tube.

12. ACUTE OTITIS MEDIA
Stage of complication
Stage of resolution
Stage of suppuration
Stage of presuppuration
Stage of tubal occlusion

13. ACUTE OTITIS MEDIA
1) STAGE OF TUBAL OCCLUSION -
• DECRESED
Air fluid level
• DECRESED & INCRESED RESPECTIVELY
• RETRACTED
Intratympanic
pressure
TM
• OCCLUDED
• HYPEREMIA & CONGESTED
ET TUBE
MUCOSA

14. ACUTE OTITIS MEDIA
 Symptoms:
 Deafness & ear ache , but are not marked.
 There is generally no fever .
 SIGN -
 TM retracted.
 Fore shortened handle of malleus.
 No cone of light Prominent lateral process of malleus.
 Conductive deafness in tuning fork test.

15. ACUTE OTITIS MEDIA
2 ) STAGE OF PRE SUPPURATION -
Pyogenic organism invade tympanic cavity
Hyperemia of lining mucosa
Inflammatory exudate collect in middle ear
Tympanic membrane congested

16. ACUTE OTITIS MEDIA
 SYMPTOMS -
1. Marked throbbing headache
2. Adults – deafness and tinnitus
3. Children – high degree of fever and restlessness
 SIGN -
• From beginning, there is congestion of pars tensa and loss of landmarks.
• Cartwheel appearance of TM as blood vessels appear along the handle of
malleus and at periphery of TM.
• Later, whole of TM including pars flaccida becomes uniformly red. This
appearance is also termed angry looking TM.
• Tuning fork tests show conductive type of hearing loss.

17. ACUTE OTITIS MEDIA
 CART WHEEL
APPEARANCE

18. ACUTE OTITIS MEDIA
 3) STAGE OF SUPPURATION -

19. ACUTE OTITIS MEDIA
 Symptoms :
• Excruciating ear pain
• Deafness increases
• Child may run fever of
102-103 °F. This may be
accompanied by
vomiting and even
convulsion
 SIGN -
• TM appears red and bulging with loss of landmarks
• Handle of malleus may not be perceptible d/t swollen
TM
• A nipple like protrusion of TM with a yellow spot
where rupture is imminent.
• Tenderness over mastoid area may be present.
• X –rays of mastoid will show clouding of air cells
because of exudate.

20. ACUTE OTITIS MEDIA
CLOUDING OF MASTOID CELL NIPPLE LIKE PROTRUSION

21. ACUTE OTITIS MEDIA
 STAGE OF RESOLUTION

22. ACUTE OTITIS MEDIA
 Symptoms :
With evacuation of pus, earache is relieved, fever comes down and child feels
better
 SIGN -
• external auditory canal may contain blood tinged discharge which later becomes
mucopurulent.
• Usually small perforation is seen in anteroinferior quadrant of pars tensa.
• +ve light house sign: pus oozing out from perforated site in a pulsatile fashion.
• Hyperemia of TM begins to subside with return to normal color and landmarks.

23. ACUTE OTITIS MEDIA
 PIN HOLE PERFORATION LIGHT HOUSE SIGN

24. ACUTE OTITIS MEDIA
 STAGE OF COMPLICATION –
• If virulence of organism is high or resistant of pt. poor, resolution may not take place and
disease spreads beyond the middle ear
 Intra-temporal (within the confines of temporal bone) -
 Acute mastoiditis Facial paralysis Labyrinthitis Petrositis
 INTRA CRANIAL -
• Extradural abscess
• Subdural abscess
• Meningitis
• Brain abscess
• Lateral sinus thrombophlebitis
• Otitic hydrocephalous

25. ACUTE OTITIS MEDIA
 INVESTIGATION –
1. Culture & sensitivity of ear discharge.
2. X-ray of mastoid – showing clouding
3. Audiometry – shows conductive hearing loss.

26. ACUTE OTITIS MEDIA
 MANAGEMENT –
 Antibiotic therapy
• Indicated in all cases with fever and severe earache
• Ampicillin 50mg/kg/day in 4 divided dose
• Amoxicillin 40mg/kg/day in 3 divided dose
• Should be given till tympanic membrane regain
normal appearance and hearing is normal (minimum
10 days)

28. ACUTE OTITIS MEDIA
 Decongestant nasal drop : ephedrine 1% in adult and 0.5% in children or
oxymetazoline or xylometazoline – used to relieve Eustachian tube edema and
promote ventilation
 Oral nasal decongestant :pseudo ephedrine (Sudafed) 30 mg twice daily
or a combinations of decongestant and antihistaminic (triominic)
 may achieve the same result without resort to nasal drops which are difficult to
administer in children.

29. ACUTE OTITIS MEDIA
 Analgesics and antipyretics : to relieve pain and bring
temperature down
• Ear toilet : discharge in ear – dry mopped with sterile cotton buds and wick
moistened with antibiotics may be inserted.
 Dry local heat : to relieve pain.

30. ACUTE OTITIS MEDIA
 SURGICAL M/M – MYRINGOTOMY.
 INDICATION OF MYRINGOTOMY -
1. Symptoms are not relieved by antibiotics
2. TM bulges significantly
3. TM perforation is too small
4. Incomplete resolution( persistent conductive hearing loss)
5. Persistent effusion beyond 12 weeks

32. OTITIS MEDIA WITH EFFUSION
• It is chronic accumulation of mucus within the middle ear & in
mastoid air cell system.
• Duration >12 weeks.
• m/c cause of acquired conductive hearing loss in children.
• Synonyms
o Glue ear .
o Serious otitis media.
o Chronic nonpurulent otitis media.

33. OTITIS MEDIA WITH EFFUSION
 When childhood OME is preceded by an episode of acute otitis media, however,
this typically follows a viral upper respiratory tract infection, associated
inflammation and infection of the adenoid, secondary bacterial infection with a
cascade of inflammatory mediators, upregulation of mucin genes and effusion
from the middle ear mucosa.

34. OTITIS MEDIA WITH EFFUSION
• OME is caused by inflammation of this epithelium in the Eustachian tube
& the hypotympanum.
• Eustachian tube and anterior mesotympanum are lined by ciliated,
pseudostratified columnar respiratory epithelium & contains both goblet cells and
mucus-secreting glands
• Inflammation of the epithelium & production of a serous or mucus effusion results
in OME.

35. OTITIS MEDIA WITH EFFUSION
 In established OME, the flat cuboidal middle ear mastoid mucosa
replaced by thicker pseudostratified mucus-secreting epithelium with
lessly effective cilia.
 Goblet cells & mucus-secreting glands are frequently present.
 The ciliary lining be less efficient at moving the secretions into the
nasopharynx than normal. The submucosa is oedematous and inflamed
with dilated blood vessels and an increased number of macrophages,
plasma cells & lymphocyte.

36. OTITIS MEDIA WITH EFFUSION
CHARECTERISTICS OF EFFUSION –
 The effusion varies in composition but is predominantly made up of the
a) glycoprotein mucin,
b) secretory immunoglobulin A (IgA),
c) lysozyme,
d) interleukins
e) other inflammatory cytokines.
 The mucins that comes from the secretions that are responsible
for the viscosity of the middle ear fluids.

37. OTITIS MEDIA WITH EFFUSION
PREVALANCE –
 Bimodal in presentation, with the
 first and largest peak found in approximately 20% of children aged 2 years.
 Second peak of approximately 16% in 5-year-old.
 Mostly OME occure in winter & summer month. reasons for seasonal variation
are the increased frequency of upper respiratory and ear infections in the
winter, including the effects of seasonal influenza, and the greater chance of
passing on infections between children because of the closer household
contact in cold weather.

38. OTITIS MEDIA WITH EFFUSION
Microbiology of OME –
 Streptococcus pneumoniae (36% of middle ear mucosal biopsy specimens
demonstrated it intracellularly)
 Haemophilus influenzae.
 Branhamella (Moraxella) catarrhalis.
 Biofilms were demonstrated in 92% of middle ear mucosal specimens of patients
undergoing ventilation tube surgery for OME.
 Communities of sessile bacteria, resistant to disruption & with a low metabolic rate,
are embedded in a matrix of extracellular polymeric substances of their own
synthesis. These communities may adhere to a foreign body or a mucosal surface
with impaired host defence.

39. OTITIS MEDIA WITH EFFUSION
ROUTES OF INFECTION –
 Eustachian tube dysfunction
• Viral upper respiratory tract infection, secondary to an allergic
reaction,Pollutents Cigarette smoke.
• Secondary to chronic nasopharyngeal infections in the adenoidal
tissue or GERD.
 Craniafacial abnormality -
• Children with a cleft palate ,even if corrected will have deficient
palatine muscles and poor ET function.
• Children with bifid uvula do not have higher incidence of OME.
• Children with Down and turner syndromes are prone to have OME.

40. OTITIS MEDIA WITH EFFUSION
 GERD
• Its common in children.
• during swallowing, fluid can travel from the nasopharynx via the
Eustachian tube into the middle ear.
• Pepsin was first identified in middle ear effusions in 2002.Bile acids have
also been identified in samples of middle ear fluid in children with OME.
• Helicobacter pylori, confirmed by PCR assay, has been detected in
middle ear effusions
 Allergy - not a risk factor for OME.

41. OTITIS MEDIA WITH EFFUSION
 GENETIC FACTOR - There is greater concordance In monozygotic set in
number and duration of OME episodes than in dizygotic sets.
 RACE - Prevalence is different in different race.
 GENDER – equal in both sex.
 SMOKING – there is noted a temporal decline in consultations for otitis media,
which was attributed to an increase in smoke-free households.
 Bottle feeding,
 Feeding while supine,
 Having a sibling with otitis media,
 Attending day care,

42. OTITIS MEDIA WITH EFFUSION
CLINICAL FEATURE –
 Quiescent phase – Asymptomatic
 Covert or overt hearing loss
 Impaired speech and language development
 Behavioral changes
 Indirect symptoms of hearing loss (changes with position).
 Otalgia – due to secondary infection
 Features of associated URI, Nasal pathologies

43. OTITIS MEDIA WITH EFFUSION
DIAGNOSIS –
 HISTORY - Parents give history of ear problem (decreased hearing),
recurrent URI, mouth breathing and snoring ,such child can
have recurrent OME.
 EXAMINATION –
 OTOSCOPY
 TYMPANOMETRY
 AUDIOMETRY – tuning fork test but above 5yr of age.
 RADIOLOGY – MASTOID & ADENOID

44. OTITIS MEDIA WITH EFFUSION
OTOSCOPY –
 Initial diagnosis by Otoscopy,prefreably Pneumatic Otoscopy.
 The otoscopy findings are mainly different combinations of
retraction of the pars tensa and variations in its colour.
 Sensitivity ranges from 85% to 93% and its specificity from 71% to 89%.

45. OTITIS MEDIA WITH EFFUSION

46. OTITIS MEDIA WITH EFFUSION

47. OTITIS MEDIA WITH EFFUSION

48. OTITIS MEDIA WITH EFFUSION

49. OTITIS MEDIA WITH EFFUSION
TYMPANOMETRY - For more than 30 years, tympanometry using an automated
impedance meter has been widely available as a method of detecting OME.
A modification of the Jerger classification is the most commonly used in clinical
practice.
a type B tympanogram is frequently associated with OME
a type A is infrequently associated with OME
a type C falls in between.
ACOUSTIC REFLECTOMETRY - Unfortunately, the sensitivity and specificity of the test
is poorer than tympanometry.

50. OTITIS MEDIA WITH EFFUSION
• MANAGEMENT – OME is having high spontaneous recovery rate &no long term
sequelae.
• Definitive treatment is Myringotomy with Ventilation tube insertion +
adenoidectomy.
 I. Counselling and hearing tactics
 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.

51. OTITIS MEDIA WITH EFFUSION
 MEDICAL MANAGEMENT –
• Antibiotics
o Benefits in first two weeks and long term is not recommended (>6 weeks).
• Nasal Decongestants
o No Significant effect.
• Mucolytes
o No Significant result.
• Nasal topical Steroids
o No difference in resolution.
• Systemic Steroids
o Not Recommended.

52. OTITIS MEDIA WITH EFFUSION
SURGICAL MANAGEMENT –
MYRINGOTOMY & INSERTION OF VENTILATION TUBES –
o Posterosuperior insertion is not recommended –damages the Ossicular Chain
o No difference in radial or circumferential inscion or anterosuperior & anteroinferior
position.
o To maximize the duration-insertion in anteroinferior is recommended .
o Made with Teflon,Silicone,Titanium,Gold.
o Aspirate as much of the middle ear fluid as possible through the myringotomy
before inserting VT, there is no evidence that is required.
o Topical preparations are used to prevent tube block with blood or infection.

53. OTITIS MEDIA WITH EFFUSION
 Ventilation Tubes –
Synonyms -
• Myringotomy tube,
• Tympanostomy tube
• Pressure equalization (PE) tube.
Types-
1. Grommets(dumbbell shaped)-
Short stay tubes that gets extruded
within 6 months.
• Shephard’s grommet
• Armstrong’s grommet
• Donaldson’s grommet
• Shah’s grommet
2. T-tube (‘T’shaped) -
For long term purposes that stays at
least 1-2 years.

54. OTITIS MEDIA WITH EFFUSION
 A- SHEPHARD’S GROMMET
 B- ARMSTRONG’S GROMMET
 C- DONALDSON’S GROMMET
 D- SHAH’S GROMMET
 E- T TUBE

55. OTITIS MEDIA WITH EFFUSION
• 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.
• 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.

56. OTITIS MEDIA WITH EFFUSION
COMPLICATION OF VT TUBE –
 Dislodgement
 Blockage ( 9% without antibiotics &1% with antibiotics)
 Otorrohoea -
• acute otorrhoea 9%
• Recurrent otorhoea 7%
• Chronic otorrhoea 3%
 Perforation -
• Short term incidence 2%
• Long term incidence 17%

57. OTITIS MEDIA WITH EFFUSION
 Adenoidectomy -
• Mechanism in resolving OMEis Unclear.
• Hypothesis being, it removes a chronic source of infection in the
nasopharynx.
• Suction diathermy ablation is much better than Conventional
(blind Curettage) adenoidectomy.
 OUTCOMES –
• VT alone will improve hearing by 12 dB.
• Adenoidectomy has additional effect of3-4 dB.

58. ACUTE NECROTIZING
OTITIS MEDIA

59. ACUTE NECROTIZING OTITIS MEDIA
 It is special form of acute suppurative otitis media.
 Common in infants & children following scarlate
fever,measles ,pneumonia,influenza or other systemic
illness.
CAUSE –
 Measles
 Scarlet fever
 Typhoid fever

60. ACUTE NECROTIZING OTITIS MEDIA
ORGANISM – Beta hemolytic streptococcus & virus.
PATHOLOGY – true necrosis of considerable areas of soft
tissue and some times bone due to the virulent micro
organism the most vulnerable areas to the toxin of the
micro-organism are those with poorest blood supply.
Thus the first tissue to succumb is the central kidney
shaped area of pars tensa.

61. ACUTE NECROTIZING OTITIS MEDIA
SIGN – near total perforation or kidney shaped
perforation with foul smelling purulent discharge.
Treatment – penicillin injection as early as possibly
gamma globulines may help
cortical mastoidectomy

62. ACUTE NECROTIZING OTITIS MEDIA
END RESULTS OF ANOM –
 Healing of central perforatione with scar
 Healing of central perforatione with permanent conductive
hearing loss.
 Permanent cental perforation with conductive hearing loss.
 Permanent perforation with chronic mucoid discharge.
 Formation of cholesteatoma.

64. Definition
 Chronic otitis media (COM) implies a permanent abnormality of the pars
tensa or flaccida, most likely as a result of- (Scott Brown)
earlier acute otitis media,
negative middle ear pressure
otitis media with effusion.
 COM is a long standing inflammation of mucoperiosteum of middle ear
cleft
• characterized by -
– By ear discharge
– A permanent perforation.

66. Types of COM
 Tubotympanic (safe or Benign type) -
• Involves anteroinferior part of middle ear cleft.
• Eustachian tube and mesotympanum
• Associated with a central perforation.
• There is no risk of serious complications.
 Atticoantral (unsafe or Dangerous type) -
 Involves posterosuperior part of the cleft (I.E. Attic, antrum and mastoid)
• Associated with an attic or a marginal perforation.
• The disease is often associated with a bone eroding process such as cholesteatoma,
granulations or osteitis.
• Risk of complications is high in this variety.

68. CLASSIFICATION OF COM

69. COM
MUCOSAL
ACTIVE (PERFORATION +
OTTORRHEA)
HEALED
INACTIVE (DRY
PERFORATION
SQUAMOSAL
INACTIVE
(RETRACTION,ATELECTA
SIS,EPIDERMIZATION
ACTIVE
(ACQUIRED
CHOLESTEATOMA)

70. MUCOSAL COM

71. AETIOLOGY OF COM
 Repeated episodes of AOM & OME.
 Genetics & race – in the developed world, is highest in Eskimos,
American Indians, New Zealand Maoris and Australian Aborigines.
 Environment – low socioeconomic status.
 Upper respiratory infection
 Gastro esophageal reflux disease
 Cranio facial abnormality – cleft palate- hypoplastic TVPM - ETD
 Immune deficiency- AIDS is highly associated to COM

72. AETIOLOGY OF COM
 Eustachian tube dysfunction - arises
from
 Inflammatory disorders – cause mucosal
edema & mucus production d/t allergic
condition,LPRD/ GERD,smoking related ciliary
dysmotility.
 Muscular abnormalities- mayopathies that
affects palatal musculature & consequently
the dynamic excurtion of of orifice.
 Anatomic factor – obstruction of tubal orifice
d/t prominent adenoid tissue,synechiae from
nasopharyngeal mass.

73. MUCOSAL COM
 INACTIVE MUCOSAL - There is
permanent perforation of the
pars tensa but the middle ear
and mastoid are not inflamed.
 The mucocutaneous junction
is usually located at the
margin of perforation which
can extend up to the fibrous
annulus.

74. MUCOSAL COM
 ACTIVE MUCOSAL COM (PERFORATION
WITH OTORRHOEA) -
Chronic inflammation within the mucosa
of the middle ear and mastoid with varying
degrees of
oedema,
submucosal fibrosis
hypervascularity
an inflammatory infiltrate including
lymphocytes, plasma cells and histiocytes
which collectively form mucopus.

75. MUCOSAL COM
 ETIOPATHOGENESIS –
- Repeated attack of AOM starts in childhood which causes
perforation & becomes permanent and permits repeated infection from
the external ear.
• Ascending infections via the eustachian tube.
– Infection from tonsils, adenoids and infected sinuses may be
responsible for persistent or recurring otorrhoea.
 Persistent mucoid otorrhoea is sometimes the result of allergy to
ingestants such as milk, eggs, fish, etc
 Single episode of measles (pre-immunization era).

76. MUCOSAL COM
 INFECTION/MICRO-ORGANISM – pus culture shows mixed infection aerobic
& anaerobic micro organism both.
• Common aerobic organisms -
– Pseudomonas aeruginosa
– Proteus
– Escherichia coli
– Staphylococcus aureus
• Anaerobes include Bacteroides fragilis and anaerobic
Streptococci.

77. MUCOSAL COM
PATHOLOGY –
1. Perforation of pars tensa- Central perforation
Histological degeneration of the tympanic membrane occurs in the outer
and inner fibrous layers of the lamina propria & in the submucosal layer.
Reduce the elastic properties of the tympanic membrane making it more
susceptible to chronic perforation.
2. Middle ear mucosa -
oedematous pale & velvety.
increase in the number of goblet cells and basal hyperplasia in the
middle ear epithelium.
Granulation tissue can occur and this is often clinically described as
‘aural polyps’.

78. MUCOSAL COM
3. Ossicular chain - It is usually intact and mobile but may show some
degree of necrosis.
- The affected ossicles typically show areas of hyperaemia with
proliferation of capillaries and prominent granulation tissue.
- The long process of the incus >> stapes crura >> body of incus &
manubrium are involved in decreasing order of frequency.

79. - resorption of bone occure d/t activation of osteoclastic cell
which is primed with recepter activator NF-kB(RANKL). After
activation a variety of cytokines release like TNF-alfa,IL-
1a,IL-1b, IL-6, INF-B, PTHrP, nitric oxide type 2.
- Bacterial cell wall structure (Lipopolysaccerides) also
stimulate bone resorption.
4. MASTOID BONE – showing sclerosis.

80. MUCOSAL COM
 CLINICAL FEATURE –
1. Ear discharge. It is non-offensive, mucoid or mucopurulent, constant
or intermittent, whitish yellow, odorless,not blood stained.
2. Hearing loss - It is conductive type(25 to 45 dB), rarely exceeds 50
dB. But might be normal in small & dry perforation.
3. Perforation - Always central
4. Middle ear mucosa - It is seen when the perforation is large.

81. MUCOSAL COM
INVESTIGATION -
1. Examination under microscope
2. Audiogram.
3. Culture and sensitivity of ear discharge.
4. PATCH TEST –when HL is near about 40-50 dB.
5. IMAGING - Mastoid X-rays/CT scan temporal bone.

82. MUCOSAL COM
EXAMINATION UNDER MICROSCOPE -
• Confirmation of otoscopic findings.
• Epithelial migration atperforation margin.
• Cholesteatoma & granulations.
• Adhesions & Tympanosclerosis.
• Assessment of Ossicular chain
integrity.
• Collection of discharge forculture
sensitivity.

83. MUCOSAL COM
AUDIOMETRY – Pure tone audiometry. It shows conductive HL The
degree of air-bone gap depends on size of perforation & erosion of
ossicular chain.
– Presence of hearing loss.
– Degree of hearingloss.
– T
ypeof hearing loss.
– Hearing of otherear.
– Record to compare hearing post-operatively.
– Medico legal purpose.

84. MUCOSAL COM
 X- RAY/CT SCAN OF TEMPORAL BONE –
- x – ray of mastoid shows – sclerosis
- CT scan with 1.5 mm section in both axial & coronal plain
of temporal bone to be done.

85. MUCOSAL COM
 PATCH TEST –
– Do pure tone audiometry :- for hearingthreshold
– Put Aluminum foil patch overT
.M.perforation.
– Repeat pure tone audiometry.
• Hearing improved  Ossicular chain intact & mobile.
• Hearing same / worse  Ossicular chain broken or
fixed.

86. MUCOSAL COM
MANAGEMENT -
1) INACTIVE COM - Dry perforations that are symptom-free do not usually
require closure. usually recurrent episodes of acute infection with
perforation of the tympanic membrane, which initially heals successfully
within a few days, but after a variable number of attacks the tympanic
membrane fails to heal. This is regarded as a result of failure of the blood
supply to the perforation edges due to endarteritis.
METHOD TO CLOSE TM PERFORATION –
 Chemical cautery with silver nitrate
 Fat grafting
 Tympanic membrane patcher
 Myringoplasty

87.  ACTIVE MUCOSAL COM –
1) NON SURGICAL M/m- aural toilet.
topical antibiotics (with or without steroid)
1) SURGICAL M/m – tympanoplasty.
adjuvant cortical mastoidectomy

88. SQUAMOUS EPITHELIAL COM
 DEFINITION – chronic inflammatory condition of middle ear cleft which involve
postero-superior part of meso tympanum (attic,antrum) or pars tensa ,with
cholesteatoma.
 It is dangerous bcoz of higher chance of complication d/t bone erosion.
 It is of two types –
 Inactive squamosal com (Retraction)
 Active squamosal com (Cholestiatoma)

90. INACTIVE SQUAMOUS COM
RETRACTION / ATELECTESIS / EPIDERMIZATION
 Retraction of the pars flaccida or pars tensa (usually posterosuperior)
which has the potential to become active with retained debris.
 Negative static middle ear pressure can result in retraction
(atelectasis) of the tympanic membrane.
 ‘EPIDERMIZATION’ is a more advanced type of retraction and refers to
replacement of the middle ear mucosa by keratinizing squamous
epithelium without retention of keratin debris.
 Epidermization remains quiescent & does not progress to
cholesteatoma or active suppuration.

91. INACTIVE SQUAMOUS COM
What is retraction of TM?
 Invagination of TM into middle ear.
 It occurs due to negative middle ear pressure.
 Classification for retraction –
For pars tensa – Berco & Sade
For pars flaccida – Tos et al

92. INACTIVE SQUAMOUS COM
 Berco & Sade classification

94. INACTIVE SQUAMOUS COM
 For pars flaccida – Tos et al.
 Stage 1- the pars flaccida is dimpled and more
retracted than normal but not adherent to the
malleus.
 Stage 2 - the retraction is adherent to the neck
of the malleus and the full extent of the
retraction can be seen.
 Stage 3 - part of the retraction is out of view
and there may be partial erosion of the bony
attic wall.
 Stage 4 - there is definite erosion of the attic
wall with the full extent of the retraction being
uncertain because it is out of view.

96. ACTIVE SQUAMOUS COM
 ACQUAIRED CHOLESTEATOMA-
 It is end stage of retraction of pars
tensa /pars flaccida.
 Retraction of the pars flaccida or
tensa that has retained squamous
epithelial debris and is associated
with inflammation and the
production of pus, often from the
adjacent mucos.

97. ACTIVE SQUAMOUS COM
 CHOLESTEATOMA - first coined by the German physiologist Johannes Muller in 1838.
 A benign keratinizing epitheliallined cystic structure found in the middle ear and
mastoid. It can cause destruction of the local structures – ossicular chain and otic
capsule, thereby leading to complications such as hearing loss, vestibular dysfunction,
facial paralysis and intracranial disease or infection.
• Normally, middle ear cleft is lined by different types of epithelium in different
regions
• It is the presence of keratinizing squamous epithelium in the middle ear or mastoid.
• “Skin in the wrong place.” coz histologically the sq.epithelial lining or matrix of
cholesteatoma is similar to the skin.

98. ACTIVE SQUAMOUS COM
 May develop anywhere within pneumatized portions of the
temporal bone but most frequent position -
1. Middle ear
2. Mastoid cavity
 Essentially, cholesteatoma consists of two parts:
a) the matrix, which is made up of keratinizing squamous
epithelium resting on a thin stroma of fibrous tissues.
b) a central white mass, consisting of keratin debris
produced by the matrix .

100.  How it destruct the bone ?
 The interplay between the epithelium of cholesteatoma & the surrounding stroma is key to
understanding its destructive effects.
 defects in the regulation of epidermal growth factor receptor (EGFR) system, IL-1 and TGF-α &
MMP-9 cause bony destruction
 As the cholesteatoma contacts bone, the normal mucosal lining degenerates & inflammatory
mediators of destruction such as macrophages, monocytes & osteoclasts begin to appear in
large numbers. Multinucleated osteoclasts responsible for bone resorption.
 Lipopolysaccharides stimulate osteoclastic bone resorption by inducing maturation of pro-
osteoclastic cells, but only if these cells are primed with a receptor activator NF-kB (RANKL).

101. ACTIVE SQUAMOUS COM
 TYPES OF CHOLESTEATOMA –
 CONGENITAL
 PRIMARY ACQUIRED
 SECONDARY ACQUIRED
 TERTIARY ACQUIRED
 ORIGIN OF CHOLESTEATOMA-
1. PRESENCE OF CONGENITAL CELL REST
2. INVAGINATION / RETRACTION POCKET THEORY – WITTMACCK’S theory
3. BASAL CELL HYPERPLASIA – RUEDI’S THEORY
4. EPITHELIAL INVASION THEORY – HABERMANN’S THEORY
5. SQUAMOUS METAPLASIA THEORY – SADE’S THEORY

102. ACTIVE SQUAMOUS COM
• CONGENTAL CHOLESTEATOMA - It arises from the embryonic epidermal cell
rests.
• 3 important sites:
– Middle ear
– Petrous apex
– Cerebellopontine angle
 LEVENSON’S CRITERIA –
a. Normal tympanic membrane (pars tensa & flaccida )
b. A white mass medial to normal TM.
c. No prior h/o otorrhea or perforation.
d. No prior otologic procedure.
e. Prior bouts of otitis media not ground for exclusion of congenital disease.

103. ACTIVE SQUAMOUS COM
 It may sometimes be discovered on routine
examination of children or at the time of
myringotomy.
 It may also spontaneously rupture.
 Present with a discharging ear
indistinguishable from a case of chronic
suppurative otitis media.
 Pt presents with painless whitish mass behind
intact TM varing degree of conductive
hearing loss depending upon size.
 It does not erode the scutum in contrast to
acquired cholesteatoma.
Anterosuperior > posterosuperior

104. ACTIVE SQUAMOUS COM
 Primary acquired cholesteatoma – no h/o previous otitis media or pre existing
perforation.
 Following theory supports its pathogenesis-
 INVAGINATION / RETRACTION POCKET THEORY (Wittmack’s theory) –
 d/t eustachian tube dysfunction pars flaccida retracted medialy on top of
neck of malleus,forming retraction pocket.
 Normal migratory pattern of the tympanic membrane epithelium altered by
retraction pocket
 Enhances potential accumulation of keratin.
 These defect have the appearance of marginal perforation.

105. Retraction pocket in pars flaccida or Postero-superior quadrant of pars tensa d/t ET dysfunction

106. ACTIVE SQUAMOUS COM
 BASAL CELL HYPERPLASIA (Ruedi’s theory) –
 According to this theory epithelial cell of pars flaccida invade the sub
epithelial tissue by proliferating columns of epithelial cell.

107. ACTIVE SQUAMOUS COM
 SQUAMOUS METAPLASIA THEORY (Sade’s theory) –
 According to this theory simple squamous epithelium of middle ear cleft
undergo a metaplasia transformation into keratinizing squamous
epithelium.

108. Attic cholesteatoma Attic cholesteatoma with granulation

109. ACTIVE SQUAMOUS COM
 SECONDARY AQUIRED CHOLESTEATOMA –
 It occurs in already pre existing diseased ear. This is often associated with
posterosuperior marginal perforation or sometimes large central perforation.
 EPITHELIAL INVASION THEORY (Habermann’s theory) –
 According to this theory keratinizing sq. epithelium from surface of TM invade into
the middle ear from perforation which follow the concept of “contact guidance &
contact inhibition ”.
 Transformation of middle ear mucosa into keratinizing squamous epithelium due
to infection via TM perforation.

110. ACTIVE SQUAMOUS COM

111. ACTIVE SQUAMOUS COM
Secondary cholesteatoma

112. ACTIVE SQUAMOUS COM
 TERTIARY ACQUIRED CHOLESTEATOMA –
 MECHANISM -
 Epithelial entrapment in fractureline.
 Ingrowth of epithelium through fracture line.
 Traumatic implantation of epithelium into middle ear.
 Entrapment of epithelium medial to E.A.C. Stenosis.

113. ACTIVE SQUAMOUS COM
• It invades the surrounding structures, first the path of least resistance, and
then by enzymatic bone destruction.
• An attic cholesteatoma may extend
– Backwards into the aditus, antrum and mastoid.
– Downwards into the mesotympanum.
– Medially, it may surround the incus and/or head of malleus.
– Cause destruction of ear ossicles.
– Erosion of bony labyrinth.
– Canal of facial nerve.
– Sinus plate or tegmen tympani.

114. ACTIVE SQUAMOUS COM
• Attributed to various enzymes such as
– Collagenase,
– Acid phosphatase and proteolytic enzymes,
• Liberated by osteoclasts and mononuclear inflammatory cells,
• Seen in association with cholesteatoma.

116. PATHOLOGICAL CHANGES –
1. T.M.perforation (marginal or attic)
2. T.M.retraction pocket (attic or P
.S.Q.)
3. Cholesteatoma formation
4. Ossicles: destruction
5. Middle ear mucosa: edematous, red,polypoid
6. Aural polyp: red,fleshy
7. Osteitis & granulation tissueformation
8. Mastoid bone: erosion,sclerosis

117. CLINICAL FEATURE -
 Ear discharge: scanty, purulent, continuous, foul-smelling, blood-stained
 Hearing Loss: conductive or sensori-neural
 T
.M.perforation: marginal /attic /total
 T
.M.retraction pocket: attic orP.S.Q.
 Cholesteatoma flakes.
 Aural polyp, osteitis & granulation tissue.

118. INVESTIGATION –
 EXAMINATION UNDER MICROSCOPE
 AUDIOGRAM
 X-RAY MASTOID
 C/S OF EAR DISCHARGE
 CT scan OF TEMPORAL BONE

119. NORMAL CELLULAR MASTOID SCLEROTIC MASTOID

120. DIPLOIC MASTOID ATTIC BONE EROSION

121.  CT TEMPORAL

122. MANAGEMENT –
 MEDICAL – limited disease in elderly patients with comorbidities
topical ear drops with frequent suction & cleaning.
 SURGICAL – CANAL WALL UP MASTOIDECTOMY
CANAL WALL DOWN MASTOIDECTOMY (MRM & RM)

123. CANAL WALL UP
MASTOIDECTOMY –
 Preservation of posterior canal
wall during simple
mastoidectomy with or without
posterior tympanotomy (facial
recess approach).
 Cholesteatomas of attic,
antrum, post.
mesotympanum with
adequate ME and mastoid
aeration.

124. CANAL WALL DOWN
MASTOIDECTOMY –
 Removal of post. canal wall to level
of vertical facial nerve.
 Creation of mastoid cavity
with exteriorization of
mastoid into EAC.
 Scutum removed with obliteration
of epitympanum and removal of
malleus head and incus.
 MRM ME space maintained while radical
mastoid eliminates ME space and
obliterates eustachian tube.

125. COMLICATION OF COM
 MASTOIDITIS
 FACIAL PALSY
 LABYRINTHITIS
 LABYRINTHITIS FISTULA
 PETROSITIS
 POSTAURICULAR
FISTULA
 SUBPERIOSTEAL ABCESS
 BEZOLD ABCESS
 CITELLIs ABCESS
 LUCs ABCESS
 Zygomatic abcess
 Subcutaneous abcess
 Subperiosteal abcess
 Meningitis
 Brain abcess
 Subdural abcess
 Extradural abcess
 Venous sinus
thrombophlebitis
 Otitic hydrocephalous
INTRATEMPORAL
EXTRA TEMPORAL
( EXTRACRANIAL)
EXTRA TEMPORAL
( INTRACRANIAL)

126. GRANULOMATOUS DISEASE OF ME
 TUBERCULOSIS
 WEGENER’S GRANULOMATOSIS
 LANGERHAN’S CELL HISTIOCYTOSIS
 MYCOTIC DISEASE

127. GRANULOMATOUS DISEASE OF ME
TUBERCULOSIS –
Tuberculosis is an infection caused by Mycobacterium tuberculosis and is
spread via respiratory droplets.
ROUTE OF INFECTION - Spread into the middle ear and mastoid occurs
either through direct extension of the upper airway infection via the
Eustachian tube, or by hematogenous seeding.
Clinical feature –
 painless serous or purulent drainage
 conductive hearing loss.

128. GRANULOMATOUS DISEASE OF ME
EXAMINATION –
 Otoscopy - tympanic
membrane with
multiple perforations
or one coalescent
perforation.
Intraoperative
findings include thick,
pale granulation tissue.

129. GRANULOMATOUS DISEASE OF ME
 DIAGNOSIS - included in the differential diagnosis of a
draining ear that is resistant to the usual topical therapy.
- Pus culture sensitivity(slow growing usually requiring at
least 6 weeks for culture results to become positive)
- Real time PCR
 HISTOPATHO FINDING – caseating granuloma.
 MANAGEMENT – anti tubercular drug for 6 month to one year.

130. GRANULOMATOUS DISEASE OF ME
MYCOTIC DISEASE
Fungal infectioin & inflammation of middle ear.
1) Superficial
2) Invasive
Superficial -
Involve colonization in EAC & middle ear (m/c site)
M/C fungal pathogen – candida & aspergillus
Symptoms – itching,otorrhea & otalgia.
On otoscopy – spores are visible as white or black colony
T/t – debridement with topical antifungal agent (clotrimazole1% with
steroid)

131. GRANULOMATOUS DISEASE OF ME
INVASIVE FUNGAL INFECTION –
 Pathogen – Cryptococcus
Aspergillous
Mucor
 Cryptococcus typically presents with neurologic symptoms. headache,
confusion, depression, and agitation.
 Aspergillosis most often begins as a pulmonary infection with direct
seeding of the Eustachian tube and middle ear.
 Mucormycosis involves the sinonasal cavity and orbit and follows a
fulminant course.

132. GRANULOMATOUS DISEASE OF ME
 In invasive cases, Fungi of the order Mucor are most commonly
implicated, followed by Aspergillus and Cryptococcus.
 All three pathogens have been found to involve the temporal bone
 Clinical feature – Acute severe otalgia along with otorrhea
Hearing loss, either sensorineural or conductive.
Vertigo, facial paralysis & other cranial
neuropathies.
 Critical features of invasive fungal infections are vascular thrombosis
and widespread tissue necrosis.

133. GRANULOMATOUS DISEASE OF ME
 Invasive fungal infections of the temporal bone include middle-ear
involvement of the submucosa and tympanic membrane as well as
infiltration of the nerves in the internal auditory canal, the
membranous labyrinth, Rosenthal's canal with loss of cochlear
neurons, and labyrinthine artery occlusion.
 Treatment - surgical debridement and systemic antifungal therapy,
such as amphotericin-B.
 Invasive fungal infections carry a high morbidity and mortality.

134. GRANULOMATOUS DISEASE OF ME
WEGENER GRANULOMATOSIS –
 first described by Klinger in 1931, but Wegener is credited as the first to
report it as a distinct clinical entity.
 An idiopathic, granulomatous necrotizing vasculitis.(capillaries and small
arterioles).
 female predominance.
 peak age at onset ranges from 45 to 65 years.
 Organ involved- kidneys, lungs, and upper aerodigestive tract.
 Otic involvernent occurring in 19 to 56 % of patients.

135. GRANULOMATOUS DISEASE OF ME
Pathology – antibody c-ANCA (antineutrophil cytoplasmic
antibody) forms against complementary peptide protinase 3
(PR3).
 Antibody production is stimulated by exogenous infectious
agent specially s.aureus which has a protein with a peptide
sequence quite similar to that of PR3.
 The c-ANCA then causes damage by activating neutrophils,
releasing free radicals and lytic enzymes.

136. GRANULOMATOUS DISEASE OF ME
 Triad - upper respiratory tract granulomas, necrotizing vasculitis, &
glomerulonephritis.
 Diagnosis - Sinonasal biopsies with serum marker c-ANCA.
 Clinical feature - conductive hearing loss,
sensorineural hearing loss,
tinnitus,
vertigo,
otalgia,
facial nerve paresis,
otorrhea.

137. GRANULOMATOUS DISEASE OF ME
 O/E - mucosa has prominent, often pale, edematous changes.
granulation tissue in the middle-ear space, at the Eustachian tube orifice, along
with fibrous deposits in the submucosal layer of the middle ear & mastoid with
necrotizing blood vessels surrounded by leucocytic infiltration. Also, proteinaceous
material in the perilymphatic space, hair cell degeneration, edema of the spiral
ligament, ossification of the cochlear turns, & thickening of the round-window
membrane with invasion of the membranous labyrinth have been documented.

138. TREATMENT – immunomodulator like cyclophosphamide or
methotrexate, combined with glucocorticoids.
 Antistaphylococcal antibiotics such as cotrimazole or trimethoprim
have had mixed long-term results.
 the T-cell and B-cell inhibitor of differentiation, deoxyspergualin,
showed promise in refractory cases leading to complete or partial
remission in aII cases.
 Surgical m/m - myringotomy or mastoidectomy.

139. GRANULOMATOUS DISEASE OF ME
LANGAERHANS CELL HISTIOCYTOSIS (HISTIOCYTOSIS-X) –
 involve almost any organ system and has a wide scope of possible
presentations.
 welI-circumscribed, lytic lesions with scalloped edges seen on
radiographic examination.
 Three subtypes: Eosinophilic granuloma, Hand-Schuller-Christian
disease, and Letterer-Siwe disease.

140. GRANULOMATOUS DISEASE OF ME
Eosinophilic granuloma – localized form of LCH.
 No multiorgan or systemic involvement.
 affects older children and young adults.
 Male > female.
 It is characterized by osteolytic lesions, typically of the temporal
and frontal bones. These bony lesions can be painful or
asymptomatic.
 Treatment - surgical excision, intralesional steroids, or low-dose
(around 24 Gy) radiation therapy.
 Adjuvant chemotherapy may be employed in individualized cases.
The prognosis is excellent.

141. GRANULOMATOUS DISEASE OF ME
Hand-Schuller-Christian disease –
 chronic, disseminated form of LCH which involve multiple organ
system.
 affects children and young adults.
 characterized by osteolytic lesions, typically of the mandible and
skull. 25% of patients present with the triad of an osteolytic skull
lesion, exophthalmos & diabetes insipidus due to sphenoid roof
erosion into the sella turcica.
 Treatment - surgical excision, if possible, combined with
chemotherapy and radiation therapy. The mortality rate
approximtes 30%.

142. GRANULOMATOUS DISEASE OF ME
Letterer-Siwe disease –
 the acute, disseminated form of LCH. It
 affects children less than 3 years of age. The
 presentation is acute with multiple bony lesions and extra skeletal
systemic involvement such as fever, proptosis, hepatosplenomegaly,
adenopathy, anemia, thrombocytopenia & exfoliative dermatitis.
 Treatment - chemotherapy using vinblastine, vincristine,
methotrexate, cyclophosphamide, or other cytotoxic drugs along
with intravenous high-dose corticosteroids.
 The prognosis is quite poor and the fatality rate is correspondingly
high.

143. GRANULOMATOUS DISEASE OF ME
 Otologic manifestations - can be
the initial presentation of the
disease, including otorrhea,
postauricular swelling, hearing loss,
and vertigo. Facial nerve
involvement occurs in of 3% of all
cases of LCH.
 Temporal bone involvement can
manifest as erosion of the external
auditory canal wall, mastoid cortex,
bony labyrinth, squamous bone,
zygomatic bone, or petrous bone.

144. GRANULOMATOUS DISEASE OF ME
 Histopathologically, LCH is characterized by sheets of polygonal
histiocytes (Langerhan's cells). These sheets of histiocytes rest in a
background of inflammatory cells, such as eosinophils, lymphocytes,
macrophages, multinucleated giant cells.
 The Langerhan's cell is characterized by Birbeck granules (also called X
bodies), which are trilaminar rod-shaped organelles in the nuclear
cytoplasm as seen on electron inicroscopic evaluation.
 These cells stain S-100 positive and/or CD-1a positive, and have
eosinophilic cytoplasm.
 M/m – surgical debridement.

145. REFERANCES
• Scott- Brown’s Otorhinolaryngology,Head & Neck
Surgery – 8th edition
• GLASSCOCK – SHAMBAUGH SURGERY
OF THE EAR
• OTORHINOLARYNGOLOGY 4th edition Zakir Hussain

146. Thank you….