Complications of suppurative otitis media

1. COMPLICATIONS OF
SUPPURATIVE OTITIS
MEDIA

2. Factors influencing development
of complications
1.Age
2.Poor socio-economic group
3.Virulence of organisms
4.Immune compromised host
5.Preformed pathways
6.Cholesteatoma

3. Pathways of spread of
infection
1.Direct bone erosion-hyperaemic
decalcification(a/c
infection),osteitis,cholesteatoma,granulation
tissue (c/c)
2.Venous thrombophlebitis-V of HS duralV
duralvenous sinuses supflveins of brain
3.Preformed pathways-congenital
dehiscences,patentsutures,prevousskull
fractures etc

5. Classification
complications of otitismedia
intra temporal intracranial

6. INTRATEMPORAL COMPLICATIONS
1.Mastoiditis
2.Petrositis
3.Facial paralysis
4.labyrinthitis

7. 1)mastoiditis
acute mastoiditismasked mastoiditis

8. 1a.Acute mastoiditis
When infectionspreads from the mucosa,lining
the mastoid air cells &antrum,toinvolve
bony walls of the mastoid air cell system.

9. aetiology
ASOM
High virulence,loweredresistance
Children
Βhemolytic strep,anaerobicorg

10. Pathology
1,production of pus under tension
2,hyperaemic decalcification and osteoclastic
resorptionof bony walls
both these processes combine
cause destruction &coalescence of
mastoid cells
single irregular cavity filled with pus
(EMPYEMA of MASTOID)

11. Pus may break through mastoid cortex
leading to subperiostealabscess which may
even burst on surface leading into a
discharging fistula

13. Patient presents with
1.Pain behind the ear (persistence,increasein
intensity or recurrence of pain)
2.fever(persistence or recurrence of fever)
3.Ear discharge(becomes profuse and increase
in purulence)
persistence of discharge beyond 3 wks in
a case of ASOM mastoiditis

14. signs
1.Mastoid tenderness
2.Ear discharge –mucopurulentor purulent often
pulsatile(light house effect)
3.Sagging of posterosuperiormeatalwall
4.Perforation of TM-small,widcongestion of rest of
TM
5.Swelling over the mastoid
6.Hearing loss-CHL
7.General findins-low grade fever,appearill &toxic

15. investigations
1.TC,DLC
2.ESR
3.X-ray mastoid
4.CT temporal bone
5.Ear swab

18. dds
a)Suppuration of mastoid lymph nodes
b)Furunculosisof meatus
c)Infected sebaceous cyst

19. treatment
Hospitalisationof the patient
Antibiotics
Myringotomy
Cortical mastoidectomy

20. complications
Subperiostealabscess
Labyrinthitis
Facial paralysis
Petrositis
Extraduralabscess
Subdural abscess
Meningitis
Brain abscess
Lateral sinus thrombophlebitis
Otitichydrocephalus

21. Abscesses in relation to
mastoid infection
1.Post auricular abscess
2.Zygomatic abscess
3.Bezold abscess
4.Meatal abscess(lucs abscess)
5.Citelli s abscess
6.Parapharyngeal or retropharyngeal abscess

23. 1b)Masked
(latent)mastoiditis
Slow destruction of mastoid air cellsbut
without the acute signs &symptoms
(no pain,nofever,nodischarge,nomastoid
swelling)
Mastoidectomyshow extensive destruction
of the air cells with granulation tissue and
dark gelatinous material filling the mastoid

24. Aetiology
From inadequate antibiotic therapy

25. cfs
Child
Mild pain behind the ear
Persistence of hearing loss
TM appears thick with loss of translucency
Tenderness over mastoid
Audiometry-CHL
X-ray mastoid-clouding of air cells

26. treatment
Cortical mastoidectomywith full doses of
anti biotics

27. 2)petrositis
Spread of infection from the middle ear and
mastoid to the petrouspart of temporal bone
Pneumatisationof petrousapex usually thru
2 recognisedcell tracts
1.posterosuperior tract
2.anteroinferior tract

28. cfs
GRADENIGO S SYNDROME
a)external rectus palsy(VI N)-Diplopia
b)Deep seated ear or retro orbital pain
c)persistent ear Discharge
Fever,headache,vomiting,neckrigidity,facial
paralysis,recurrentvertigo

29. diagnosis
CT scan-temporal bone(pmeumatisationof
petrousapex)
MRI(diploicmarrow-fluid or pus)

30. treatment
Cortical,radicalor modified radical
mastoidectomy
iv antibiotics

31. 3)Facial paralysis
Results either from cholesteatomaor from
penetrating granulation tissue
Destruction of bony canal
Insidious &slowly progressive

32. treatment
Urgent exploration of middle ear &mastoid
Inspect facial canal from the geniculateganglion to
the stylomastoidforamen
Cholesteatomain the bony canal is uncapped in the
area of involvement
Granulation tissue surrounding the nerve is removed
If it is actually invades the N sheath ,it is left in place
If a segment of nerve is destroyed by the granulation
tissue resection of nerve and grafting after control of
infections

33. labyrinthitis
Circumscribed diffuse serous diffuse
suppurative

34. Circumscribed labyrinthitis
(fistula of labyrinth)
Thinning or erosion of bony capsule of
labyrinth(usually HSCC)

35. cfs
c/o transient vertigo
Diagnosed by fistula test

36. treatment
Mastoid exploration
Systemic antibiotic therapy

37. Diffuse serous labyrinthitis
Diffuse intralabyrinthineinflammation
without pus formation
Reversible condition if treated early

38. aetiology
Pre –existing circumscribed labyrinthitis
In acute infections of middle ear inflamn
spreads thru annular ligament or the round
window
Following stapedectomyor fenestration
operation

39. cfs
Vertigo
Nausea
Vomiting
Spontaneous nystagmus
SNHL

40. TREATMENT
Medical
a)pt is put to bed,headimmobilisedwith
affected ear above
b)Antibiotics
c)Labyrinthine sedatives-prochloperazineor
dimenhydrinate
d)Myringotomy
Surgical
Cortical or modified radical mastoidectomy

41. Diffuse suppurative
labyrinthitis
Diffuse pyogenicinfection of labyrinth with
permanent loss of vestibular and cochlear
infections

42. aetiology
Following serous labyrinthitis
Pyogenicorganisms entering through a
pathological or surgical fistula

43. cfs
Severe vertigo with nausea and vomiting
Spontaneous nystagmus
Total loss of hearing

44. treatment
Same as for forserous labyrinthitis
Drainage of labyrinth is required if
intralabyrinthinesuppuration is acting as a
source of intracranial complications