This document discusses chronic suppurative otitis media, including factors that contribute to it, classifications, potential complications, and treatments. It covers both intratemporal complications like mastoiditis, petrositis, and facial paralysis, as well as intracranial complications such as extradural abscess, subdural abscess, meningitis, and brain abscess. For each complication, it discusses the pathology, clinical features, investigations, differential diagnosis, and treatment approaches.

1. ON OF
CHRONIC
SUPPURATIV
E OTITIS
MEDIA
Amalina Aminuddin
0820121000 67

2. • Factors
• Spread of infection
• Classification
• Sequelae
• Complications:
• Intratemporal complication
• Intracranial complication
Content

3. Factors
 Age
 Poor socioeconomic group
 Virulence of organism
 Immune-compromised host
 Preformed pathways
 Cholesteatoma

4. Pathways spread of infection
 Direct bone erosion
 Venous thrombophlebitis
 Preformed pathways
 Congenital dehiscences
 Patent sutures
 Previous skull fractures
 Surgical defects
 Oval and round windows
 Infection from labyrinth

5. Sequelae of otitis media
Perforation of
tympanic
membrane
Ossicular erosion
Atelectasis and
adhesive otitis
media
Tympanosclerosis
Cholesteatoma
formation
Conductive
hearing loss
Sensorineural
hearing loss
*Speech
impairment
*Learning
disabilities

6. Classifications
 Mastoiditis
 Petrositis
 Facial paralysis
 Labyrinthitis
 Extradural abscess
 Subdural abscess
 Meningitis
 Brain abscess
 Lateral sinus
thrombophlebitis
 Otitic hydrocephalus
INTRATEMPORAL INTRACRANIAL

8. Intratempor
al
Complicatio
n

9. A. [i] ACUTE MASTOIDITIS
 Inflammation of
mucosal lining
of antrum and
mastoid air cell
system
 mucosa bony
walls

10. Accompanies / follow
ASOM
1. Virulence of organism
2. Lowered resistance
3. Children
1. Production of pus
under tension
 Production > drainage
2. Hyperaemic
decalcification and
osteoclastic resorption
of bony wall
 Destruction,
coalescence of
mastoid air cell
[empyema of mastoid]
 subperiosteal
Aetiology PATHOLOGY

11. Clinical Features
 Pain behind the ear
 Fever
 Ear discharge
 Mastoid tenderness
 Light house effect (
pulsatile purulent
discharge)
 Sagging of
posterosuperior meatal
wall
 Perforation of tympanic
membrane
 Swelling over the
mastoid
 Hearing loss
SYMPTOMS SIGNS

12.  Blood counts
(Polymorphonuclaer
leucocytosis)
 ESR
 X-ray mastoid
 Ear swab
INVESTIGATION

13. Differential diagnosis
 Suppuration of mastoid
lymph nodes
 Furunculosis of meatus
 Infected sebaceous
cyst

14. Treatment
 Hospitalization
 Antibiotics
 Myringotomy
 Cortical
mastoidectomy
[Subperiosteal abscess,
positive resevoir sign, no
change despite medical
treatment for 48hours]

15. Complications
 Subperiosteal
abscess
 Labyrinthitis
 Facial paralysis
 Petrositis
 Extradural
abscess
 Subdural abscess
 Meningitis
 Brain abscess
 Lateral sinus
thrombophlebitis
 Otitic hydrocephalous

16. Abscesses in relation to mastoid
infection
 Postauricular abscess
 Zygomatic abscess
 Bezold abscess
 Meatal abscess (Luc
abscess)
 Behind the mastoid (Citelli’s
abscess)
 Para/retropharyngeal
abscess

17. A. (ii) MASKED (LATENT)
MASTOIDITIS
 Slow destruction of mastoid air cells with no sign
and symptoms
 Destruction of air cells + dark gelatinous material +
Eroded tegmen tympani and sinus plate +
extradural or perisinus abscess
 Aetiology :
 Inadequate dose/ duration/ frequency of antibiotic

18.  Mild pain behind ear +
Persistent hearing loss
 Thick , opaque
tympanic membrane
 Tenderness over
mastoid
 Audiometry- conductive
hearing loss
 X-ray mastoid- clouding
of air cells with loss of
cell outline
 Cortical
mastoidectomy
 Antibiotics
CLINICAL
FEATURES
TREATMENT

19. B.PETROSITIS
 Spread from middle ear
and mastoid to petrous
part of temporal bone
 Associated with acute
coalescent /latent
mastoiditis or chronic
middle ear infection

20. Pathology
 Spread thorugh:
1. Posterosuperior tract-
mastoid  runs
behind/ above
labyrinth  petrous
apex
2. Anteroinferior tract-
hypotympanum near
Eustachian tube
cochlea  petrous
apex

21. Clinical Symptoms
 Gradenigo syndrome
 External rectus palsy
 Deep-seated ear /retro-
orbital pain
 Persistent ear discharge
 Fever, headache,
vomiting, neck rigidity
 Facial paralysis,
recurrent vertigo
 Diagnosis- CT scan and
MRI

22. Treatment
 Cortical, modified radical /radical
mastoidectomy
 Find fistulous tract, curette and enlarge
 free drainage
 IV antibiotic + surgical intervention
 Only antibiotics: Initial 4-5 days of high
dose systemic antibiotics

23. C. FACIAL PARALYSIS
 Result from cholesteatoma /penetrating
granulation tissue
 Cholesteatoma destroys bony canal + edema
pressure on nerve
 Insidious but slowly progressive
 Treatment:
 Exploration of middle ear and mastoid
 Uncapped cholesteatoma
 Remove granulation tissue if not involving nerve
sheath
 Resection of nerve and grafting after infection
controlled and fibrosis matured

24. D. LABYRINTHITIS
Circumscribe
d labyrinthitis
Diffuse
suppurative
labyrithitis
Diffuse
serous
labyrinthitis

25. Circumscribed labyrinthitis
 Thinning/erosion of
bony capsule of
labyrinth
 Aetiology:
 Chronic suppurative
otitis media
 Neoplasm of middle ear
 Surgical or accidental
trauma
 Clinical Features
 Transient vertigo by
pressure on tragus/
Vasalva manoeuvre
 Diagnosis: Fistula test
 Pressure on tragus
 Siegel’s speculum
 Treatment
 Mastoid exploration and
systemic antibiotic
therapy

26. Diffuse labyrinthitis
SEROUS SUPPURATIVE
• Diffuse intralabyrinthine inflammation • Diffuse pyogenic infection
• Reversible sensorineural hearing loss • Permanent loss of vestibular and
cochlear function
• Pre-existing circumscribed labyrinthitis
• Acute infection of middle ear cleft,
• follow stapedectomy /fenestration operation
• follows serous labyrinthitis
• Mild vertigo, nausea, vomiting • Severe vertigo, nausea and vomiting
• Appears more toxic
• Quick component of nystagmus toward
affected side
• Quick component of nystagmus toward
healthy side
Treatment
 Patient is put to bed, head immobilised with affected ear above
 Antibacterial therapy
 Labyrinthine sedatives (prochlorperazine )
 Myringotomy
 Cortical /modified radical mastoidectomy

27. Intracranial
Complications

28. A. EXTRADURAL ABSCESS
 Collection of pus
between the bone and
dura
 Pathology:
 Destroyed by
cholesteatomapus
contact directly with dura
 Venous thrombophlebitis
 dura is intact
 Dura covered by
granulations / appear
unhealthy and

29.  Asymptomatic
 Persistent headache
on the side of otitis
media
 Severe pain in ear
 General malaise with
low grade fever
 Pulsatile purulent ear
discharge
 Disappearance of
headache with free
flow of pus from the
ear
 Cortical / modified
radical /radical
mastoidectomy
 Antibiotic X 5 days
 Diagnosis: contrast
enhanced CT or MRI
CLINICAL FEATURE TREATMENT

30. B. SUBDURAL ABSCESS
 Pus between dura and
archnoid
 Pathology
 Spreads by erosion of
bone and dura
/thrombophlebitic
process subdural
space and comes to lie
against the convex
surface of cerebral
hemisphere
 Clinical features
 Meningeal irritation [
headache, fever, neck
rigidity, Kernig’s sign]
 Cortical venous
thrombophlebitis [
aphasia, hemiplegia]
 Raised ICP [
papilledema, ptosis,
dilated pupil ]
 Treatment:
 burr holes /craniotomy
for drainage +IV
antibiotics

31. C. MENINGITIS
 Inflammation of pia
and arachnoid
 Most common
intracranial
complication
 Mode of infection
 Blood-borne
 Chronic ear disease
 Fever with chills and
rigors
 Headache
 Neck rigidity
 Photophobia and mental
irritability
 Nausea and vomiting
 Drowsiness, delirium or
coma
 Cranial nerve palsies and
hemiplegia
CLINICAL
FEATURES

32.  Contrast CT or MRI,
 Lumbar puncture
 CSF examination
 Antibiotics +
corticosteroids
 AOM :Myringotomy or
cortical mastoidectomy
 Cholesteoma :Radical
or modified radical
mastoidectomy
DIAGNOSIS TREATMENT:

33. D. OTOGENIC BRAIN ABSCESS
 Adult ( 50%) : CSOM with
cholesteatoma
 Child ( 25%) : acute otitis media
 Route of infection:
 Cerebral : direct extension through
tegmen /retrograde thrombophlebitis
 Cerebellar : direct extension through
Trautmann’s triangle / retrograde
thrombophlebitis
 Bacteriology:
 aerobic [ SP, PM, EC,]
 Anaerobic [ BF, HI]

34. Pathology
 Stage of invasion (initial
encephalitis)
 Headache, low grade fever,
malaise, drowsiness
 Stage of localization (latent
abscess)
 Stage of enlargement
(manifest abscess)
 Edema raised ICP
 Stage of termination
(rupture of abscess)

35. Clinical features
 1.Symptoms and
signs of raised ICP
 Headache
 Nausea and vomiting
 Level of
consciousness
 Papilloedema
 Slow pulse and
subnormal
temperature

36. 2.Localizing features
 Nominal aphasia
 Homonymous
hemianopia
 Contralateral motor
paralysis
 Epileptic fits
 Pupillary changes and
oculomotor palsy
 Headache
 Spontaneous
nystagmus
 Ipsilateral hypotonia
 Ipsilateral ataxia
 Past-pointing and
intention tremor
 Dysdiadokinesia
Temporal lobe abscess Cerebellar abscess

37.  Skull x-ray
 CT scan
 X-ray mastoids or CT
scan
 Lumbar puncture
 Antibiotics IV
 Dexamethasone or
mannitol
 Suction clearance and
topical drops
 Repeated aspiration
through a burr hole
 Excision of abscess
 Open incision of the
abscess and evacuation
of pus
 Radical mastoidectomy
INVESTIGATION TREATMENT

38. E.LATERAL SINUS
THROMBOPHLEBITIS
 Inflammation of inner wall of lateral venous sinus with
formation of intrasinus thrombus
 Occur due to acute coalescent mastoiditis, masked
mastoiditis, chronic suppuration of middle ear and
cholesteatoma
 Pathology:
Formation of
perisinus
abscess
Endophlebitis
and mural
thrombus
formation
Obliteration of
sinus lumen
and intrasinus
abscess
Extension of
thrombus

39.  Acute- haemolytic
streptococcus,
pneumococcus or
staphylococcus
 Chronic- +
cholesteatoma,
Bacillus proteus,
Pseudomonas
pyocyaneus, E. coli
and staphylococci
 Hectic Picket-fence
type of fever with
rigors
 Headache
 Progressive anaemia
and emaciation
 Griesinger’s sign
 Papilloedema
 Tobey-Ayer test,
Crowe-Beck test
 Tenderness along
jugular vein
BACTERIOLOGY
CLINICAL
FEATURES:

40.  Blood smear
 Blood culture
 CSF examination
 X-ray mastoid
 Imaging studies
 Culture and sensitivity
 Septicaemia and
pyaemic abscess in
lungs, bones, joints or
subcuteaneous tissue
 Meningitis and subdural
abscess
 Cerebellar abscess
 Thrombosis of jugular
bulb and jugular vein
 Cavernous sinus
thormbosis
 Otitic hydrocephalus
INVESTIGATION COMPLICATION

41. Treatment
 Intravenous antibacterial drugs
 C/ MR mastoidectomy and exposure of sinus
 Ligation of internal jugular vein
 Failed antibiotic and surgical treatment
 Spreading tenderness along jugular vein
 Anticoagulant therapy
 Supportive treatment

42. F.OTITIC HYDROCEPHALUS
 Raised ICP with normal CSF findings
 In children with acute/ chronic middle ear infection
 Lateral sinus thrombosis  obstruction +
extension to superior sagittal sinus  decreased
absorption
 Clinical features
Symptoms:
• Severe
headache
• Diplopia
• Blurring of vision
Signs:
• Papilloedem
a
• Nystagmus

43. Treatment:
 Reduce CSF pressure to
prevent optic atrophy and
blindness
 Acetazolamide and
corticosteroids
 Repeated lumbar
puncture / placement of
lumbar drain,
lumboperitoneal shunt
 Antibiotic therapy and
mastoid exploration