2. INTRODUCTION
Infection spreads beyond muco-periosteal lining of
middle ear cleft to involve bone & neighboring
structures like facial nerve, inner ear, dural venous
sinuses, meninges, brain tissue & extra-temporal
soft tissue
Mortality due to intracranial complication is still high
6. FACTORS
Pathogen Factors Patient Factors
High virulence bacteria Young age
Antimicrobial resistance Poor immune status
Chronic disease (DM,
TB)
Poor socio-economic
status
Lack of health awareness
12. SUBDURAL EMPYEMA
Least common complication
Non hemolytic streptococci
Inflammatory reaction underneath
dura- granulation- fibrosis-necrosis
of bone
Seropurulent – purulent collection
• Subdural space, along tentorium
cerebelli and interhemispheric
spaces
13. CLINICAL FEATURES
Dramatic presentation , rapid detioration
Severe headache, fever, drowsiness, follwed by
focal neurological symptoms
Much more rapid than brain abscess
Jacksonian fits
Hemianopia ,hemianaesthesia , aphasia
Mortality 15%
14. • along the falx
• loculated
• hypodense
• ring enhancement
• contrast imaging
• mass effect
• blunted sulci
Gd-DTPA enhanced T1 weighted MRI
CECT
15. DIAGNOSIS AND MANAGEMENT
CT scan
CSF culture sterile
With neurosurgeons
Systemic antibiotics + removal of subdural fluid
(burr hole) + ear infections acute by myringotomy
and cortical mastiodectomy
Now craniotomy abscess excision
Radical mastoidectomy after patient is stable
17. MENINGITIS
Most common intracranial complication
In children following acute and adults following
chronic infection
Mortality 5-30 %
Otogenic meningitis is most serious than
meningococcal meningitis
Hemophilus influenzae , streptococcus pneumonia
type iii – acute
Chronic – proteus and pseudomonas
Anaerobic – bacteroid
18. Routes of entry into the meninges –
haematogenous (MC)
direct extension by bone erosion (cholesteatoma, encephalocoel)
preformed channels (Hyrtl’s fissures)
labyrinth, aqueduct (suppurative labyrinthitis, Mondini
malformation)
Suspicious signs –
persistent/intermittent fever lethargy
nausea and vomiting persistent headache
irritability
Ominous signs –
visual changes ataxia
new onset seizures altered sensorium
nuchal rigidity
Associted intracranial complications in 50% of
cases
Meningitis
19. DIAGNOSIS AND TREATMENT
CSF study by LP (cytology, chemistry, smear, culture)
Broad spectrum IV antibiotics, steroids (to prevent
subsequent
hearingloss)
Myringotomy
Mastoidectomy (cholesteatoma, coalescent mastoiditis,
extension
through bone erosion, failure of maximal
medical
therapy)
24. LATERAL SINUS THROMBOPHLEBITIS
Proximal: 1. To superior sagittal sinus via torcula
Herophili hydrocephalus
2. To cavernous sinus proptosis
3. To mastoid emissary vein Griesinger’s sign
Distal: To internal jugular vein & subclavian vein
pulmonary thrombo-embolism & septicaemia
25. CLINICAL FEATURES
Remittent high fever with rigors (picket fence)
Pitting edema over retro-mastoid area & occipital
bone due to mastoid emissary vein thrombosis
(Griesinger’s sign)
Tenderness along Internal Jugular Vein
Headache
Anaemia
26. SYMPTOMS & SIGNS
High fever, swinging type
Chills precedes fever
Temperature subsides with sweating
Each fever spike due to release of fresh septic
embolus
27. INVESTIGATIONS
Queckenstedt or Tobey-Ayer test: compression of
I.J.V. rapid rise of C.S.F. pressure (50 – 100 mm
water rapid fall on release of compression. In
L.S.T. no rise / rise by only 10 – 20 mm water.
Low sensitivity and specificity
28. INVESTIGATIONS
Lumbar puncture: to rule out
meningitis
CT brain with contrast: Delta sign
or Empty triangle sign
MRI brain with contrast
MR angiography
Blood culture
Culture & sensitivity of ear
discharge
30. Algorithm for Surgery
Mastoidectomy Inspection of the sinus wall
NORMAL
(compressible, healthy-looking)
DISEASED
(inflammed, immobile, pale, opaque)
Wide bore needle aspiration
Free flow blood No blood, pus
Conservative Thrombectomy, drainage
(healthy thrombus, free flow blood)
Dry tap
34. 4 STAGES (NEELY, MAWSON)
1. Invasion or Encephalitis (1-10
days)
2. Localization or Latent Abscess
(10-14 days)
3. Expansion or Manifest
Abscess (> 14 days): leads to
raised intracranial tension & focal
signs
4. Termination or Abscess
rupture: leads to fatal meningitis
35. RAISED ICT
Seen more in cerebellar abscess
Severe persistent headache, worse in morning
Projectile vomiting
Blurring of vision & Papilloedema
Lethargy drowsiness confusion coma
Bradycardia
Subnormal temperature
40. SURGICAL MANAGEMENT
•Repeated burr hole aspirations – safer for ill patients
• Excision of brain abscess with capsule: best Tx – extensive
damage to cerebral tissue , residual neurological deficit
• Open incision & evacuation of pus
• Radical mastoidectomy after pt becomes stable
46. • More common with COM
• Cholesteatoma → tegmen dehiscence → middle or
posterior cranial fossa dural tear → CSF
leak/encephalocoel
• Iatrogenic
• Presentations
clear, colourless, watery fluid
from mastoid cavity or external auditory canal
through nose, in intact TM
middle ear/myringotomy fluid rich in glucose
• Proper exposure → temporalis muscle/fascia graft
with gelfoam compression
• Sinodural angle tear most difficult to control
• Repair via intracranial route (extradural/intradural)
47. BRAIN FUNGUS
Prolapse of brain into middle ear cavity / mastoid
cavity due to erosion of dural plate.
Common in pre-antibiotic era. Rarely seen now in
resistant infections.
Diagnosis: C.T. scan temporal bone.
Treatment: Removal of necrotic tissue, replacement
of healthy prolapsed brain into cranial cavity &
repair of bone defect.
49. • Extension of mastoid infection through the cortex and air cells into the
subperiosteal region
• Types –
Mastoid abscess (subperiosteal abscess “proper”) [MC]
von Bezold’s abscess
Luc’s (meatal) abscess
Zygomatic abscess
Citelli’s abscess
Para-/retropharyngeal abscess
• Haematogenous spread (perforators, especially in children)
• Differential diagnosis –
Mastoiditis without abscess
Suppurative lymphadenopathy
Superficial abscess
Infected sebaceous cyst
50. PATHOGENESIS
Production of pus under tension
hyperaemic decalcification
+ osteoclastic resorption of bone
sub-periosteal abscess
penetration of periosteum + skin
fistula formation
54. BEZOLD & CITELLI’S ABSCESS
Bezold: neck swelling
over sternocleido-
mastoid muscle
Citelli: neck swelling
over posterior belly
of digastric muscle
55. D/D OF BEZOLD’S ABSCESS
1. Suppurative lymphadenopathy of upper deep
cervical lymph node
2. Para-pharyngeal abscess
3. Parotid tail abscess
4. Infected branchial cyst
5. Internal jugular vein thrombosis
56. LUC’S ABSCESS
Luc: swelling in external auditory canal
Zygomatic: swelling antero-superior to pinna +
upper eyelid oedema
Parapharyngeal & Retropharyngeal: due to spread
of pus along Eustachian tube
57. CLINICAL FEATURES & TREATMENT
• Late feature of neglected COM
• CT scan (extent of the lesion, intracranial and
intratemporal complications)
• Subperiosteal abscess + cholesteatoma
Drainage + cortical mastoidectomy + IV antibiotics
• Subperiosteal abscess – cholesteatoma
Drainage + cortical mastoidectomy + IV antibiotics
Drainage + myringotomy + IV antibiotics
Aspiration + myringotomy + IV antibiotics
59. • Mastoiditis = mucositis of mastoid cavity and air
cells + effusion
part of the spectrum of uncomplicated otitis media
per se, not a complication
• Acute (clinical) mastoiditis
red, oedematous soft tissue over mastoid antrum
painful/tender
pinna directed laterally, downward and forward
loss of post-auricular crease
otorrhoea
localised reactive lymphadenopathy
pain the only presentation in adults (thicker cortex)
60. PATHOGENESIS
Aditus Blockage
Failure of drainage
Stasis of secretions
Hyperemic decalcification
Resorption of bony septa of air
cells
Coalescence of small air cells to
form cavity
Empyema of mastoid cavity
61. Disease of childhood (>2 years, peak at 6 years)
Mostly a sequelae of ASOM (Pneumococcus,
Haemophilus)
25% of coalescent mastoiditis seen in
sclerotic temporal bone with COM and
cholesteatoma
62. Fate of an inflammed mastoid cavity
Acute mastoiditis
Spontaneous resolution, perforation of tympanic
membrane
Persists
Blockage of aditus by granulation/cholesteatoma
Mastoid empyema
Acute
coalescent mastoiditis
Acidosis
Osteoclast activity
Pressure of pent-up pus
DEMINERALISATION
Subperiosteal abscess Petrositis
Intratemporal & intracranial
complications
63. SYMPTOMS & SIGNS
Otorrhoea > 3 weeks, pain behind the ear & fever
Mastoid reservoir sign: pus fills up on mopping
Sagging of postero-superior canal wall due to peri-
osteitis of bony wall b/w antrum & posterior E.A.C.
Ironed out appearance of skin over mastoid due to
thickened periosteum
Mastoid tenderness present
Blood counts , ESR raised , Mastoid cavity in X-ray &
CT scan , ear swab culture & sensitivity
68. Mastoiditis Furunculosis
H/o otitis media + -
Deafness + -
Position of pinna Down + outward
+ forward
Forward
Ear discharge Muco-purulent Serous / purulent
Sagging of EAC wall + -
TM congestion + -
Tenderness Mastoid Tragal
Post-aural lymph node - +
X-ray Mastoid Coalescence of
cells + cavity
Normal
69. MANAGEMENT
Urgent hospital admission
Broad spectrum I.V. antibiotics
Cortical mastoidectomy
No response to medical treatment in 48 hrs ,
sagging of post meatal wall
Development of new complication
Presence of sub-periosteal abscess
Myringotomy to drain out painful pus
Incision drainage of sub-periosteal abscess
70. Masked mastoiditis
Natural progress of acute mastoiditis halted by antibiotics
Middle ear apparently free from infection
Persistence of symptoms of mastoiditis
TM fails to return to normalcy
Blockage of aditus by granulation/cholesteatoma
72. Pneumatisation of the petrous pyramid
30% (anterior petrous apex), 10% (posterior petrous apex)
after 3 years of age
continuous with the middle ear cleft
POSTEROSUPERIOR/INFRALABYRINTHINE CHAIN
(attic, antrum → semicircular canal → apex)
ANTEROINFERIOR/PERITUBAL CHAIN
(hypotympanum, PT tube → cochlea → apex)
73. ACUTE PETROSITIS
• Gradenigo’s syndrome
deep-seated retro-orbital/aural pain (50%)
diplopia (lateral rectus palsy) (25%)
otorrhoea
TYPICAL GRADENIGO’S SYNDROME IS RARE
NOT PATHOGNOMONIC OF APICITIS
SIMILAR PRESENTATIONS WITH EXTRADURAL ABSCESS AT THE APEX
• Cochleo-vestibular symptoms, facial weakness,
constitutional symptoms
74. PETROSITIS
• Pneumatisation of petrous apex not
a prerequisite
ALTERNATIVE ROUTES OF SPREAD
Thrombophlebitis
Osteitis
• Long standing persistent otorrhoea
(discharging petrous
tract), with indolent symptoms
75. • Long term, high dose systemic antibiotics
• Myringotomy (± grommet), corticosteroids (neuropathy)
• Surgery –
petrous abscess, necrosis, failure of medical traetment
• Simple mastoidectomy
• Surgery in a hearing ear –
approaches following the infected air-cells
• Surgery in a non-hearing ear –
translabyrinthine & transcochlear approaches
78. • Most common complication of COM with
cholesteatoma
• Arch of the horizontal semicircular canal most
commonly affected (~90%) [nearest to the antrum
• Breach of the otic capsule
Resorptive osteitis (inflammatory mediators in COM with
cholesteatoma/granulation tissue)
Pressure necrosis (cholesteatoma mass)
• Cholesteatoma and/or granulation
79. • Presentations of labyrinthine fistula
sensorineural hearing loss
subjective episodic vertigo
positive fistula test
Tullio phenomenon
• Preoperative CT scan (30° tilted)
(57-60% sensitivity, even with 1mm cuts)
• Intraoperative diagnosis
• The presence of labyrinthine fistula to be assumed
to
be present in every case of COM with
cholesteatoma
80. Fistula test in relation to labyrinthine fistula
• Tragal pressure, Politzer bag with ear canal
adapter,
pneumatic speculum
• Conjugate ocular movements with vertigo
• Not sensitive; its absence does not rule out a
labyrinthine fistula
• False positive fistula sign (Hennebert’s sign)
intact tympanic membrane
no fistula
characteristic, though not diagnostic, of labyrinthine syphilis
• False negetive fistula sign
inadequate sealing
cholesteatoma blocking the fistula
wax in the external canal
dead labyrinth
81. Treatment of labyrinthine fistula
• Tympanomastoidectomy (CWD) + addressing the fistula
• Removal of cholesteatoma, exteriorising the fistula covered by
matrix (single sitting in open cavity/staged in closed cavity) –
prevents aggravation of SNHL by minimising tissue handling
removal of cholesteatoma itself releives pressure
keeping matrix safe until no granulation tissue lies
underneath
• Complete removal of cholesteatoma including matrix (single or
staged/2nd look sitting), repair of fistula (fascia, bone pâté)
prevention of bone erosion and infection
prevention of SNHL in the long term
82. SEROUS LABYRINTHITIS
• Translocation of toxins and inflammatory mediators
Associated perilabyrinthine infection, especially fistula
• Meningogenic (Pneumococcal mengitis → aqueducts)
Tympanogenic (round window, internal auditory canal)
• Clinical diagnosis : Sudden onset vertigo in a patient with AOM
• IV antibiotics + myringotomy ± mastoidectomy (in progressive cases)
• Hearing loss, vertigo and imbalance are reversible
83. SUPPURATIVE LABYRINTHITIS
Comparatively less common (<1%)
• Invasion of bacteria into the labyrinth
• Tympanogenic (round window, fistula)
• Haematogenic (venous channels)
• Endolymphatic hydrops (resistence of Reissner’s membrane to
bacterial invasion )
• Meningitis, intracranial (cerebellar) abscess
• Clinical diagnosis (aided by CT scan)
sudden onset severe rotatory vertigo with vomiting
profound unilateral deafness
disorder of balance
spontaneous horizontal nystagmus
• Tissue destruction and loss of functions are permanent
• IV antibiotics + myringotomy + corticosteroids + labyrinthine
sedatives + mastoidectomy ± drainage/labyrinthectomy
85. • Otitis media → 3-5% of incidences of facial palsy
• More common in children, after ASOM
• Acute onset (<1 week) in AOM, chronic protracted
course in COM
• Cholesteatoma, granulation tissue, suppurative
labyrinthitis (sequestra), petrous osteomyelitis
• Congenital petrous cholesteatoma (progressive palsy with
longstanding severe deafness, without otorrhoea)
• Facial nerve exposed by cholesteatoma mostly
escapes
palsy (epineurium replaced by matrix)
86. Causes of Facial nerve palsy
AOM
• Neurotoxic effect (inflammatory mediators, bacterial toxins
through natural dehiscences and vascular channels)
• Mass effect on the bare nerve
COM
Osteitis, erosion, direct pressure Oedema, neuropraxia,
neuronotmesis
• Cholesteatoma > granulation tissue
• Acquired Fallopian canal dehiscence
• Tubercular otitis media
87. • Clinical diagnosis
• Role of CT scan
not a routine procedure
investigation of choice
<2mm cuts, with proper exposure of tympanic cavity & facial
canal
• IV antibiotics + myringotomy ± grommet [AOM]
• Surgical exploration [COM]
CWD modified radical mastoidectomy
Removal of cholesteatoma and granulation tissue
Facial nerve decompression by removing matrix from epineurium
Nerve repair, if needed
The management