manaegement of complications of acute otitis media , anatomy , physiology , complications , diagnosis , management , By, Dr, IBRAHIM HABIB BARAKAT ( M.D. ). 00966500072975 , 0020225218374,

2. Management of
Complications of
Acute Otitis Media
Dr . Ibrahim Habib Barakat
M.D.Otorhinolaryngology

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To my family

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Anatomy of
the middle ear cavity

5. 5
Anatomy of the middle ear cavity
• Site : inside the petrous part of the
temporal bone.
• Shape: small biconcave box.
• Surfaces: roof, floor & 4 walls: ant.,
post., medial &lat.

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Middle ear cleft, Tympanum
• The middle ear cleft includes the tympanum (middle ear
cavity proper), the eustachean tube, and the mastoid air
cell system. The tympanic cavity is an air filled irregular
space contained within the temporal bone. It also contains
the three auditory ossicles (malleus, incus and stapes)
along with their attached muscles. For the purpose of
description the tympanic cavity may be considered as a
box with four walls, a roof and a floor. The corners of this
hypothetical box is not sharp.

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Surfaces of the middle ear
Roof (tegmental Formed by thin plate of bone called « tegmen tympani »
wall) It separates the middle ear cavity from the temporal lobe in the
middle cranial fossa
The floor Formed by thin plate of bone called « jugular wall »
Separates the middle ear cavity from jugular fossa containing the
sup.bulb of the I.J.V.
It is pierced by the tympanic branch of glussopharryngeal nerve.
Lateral wall Formed mainly by the ear drum
Anterior wall Contains the following structures (arranged from above downwards):
1. The opening for the canal of tensor tympani m
2. The opening for Eustachian tube.
3. A plate of bone separating the middle ear from the I.C.A in the carotid
canal.

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13. 13
Surfaces of the middle ear
Medial wall Separates the middle ear cavity from the
internal ear & shows the following features:
1. A well marked rounded bulge «
Promontary » which is produced by the
first turn of the cochlea of the inner ear.
2. Oval window: above and behind the
promontary. It is closed by the foot of the
stapes & leads to the vestibule of internal
ear.
3. Rounded window: lies below & behind the
promontry & is closed by 2ry tympanic
membrane.
4. The horizontal part of facial canal :arching
above the promontary & oval window.

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15. 15
Surfaces of the middle ear
Posterior Contains the following structures
wall (arranged from above downwards):
1.The aditus ( opening ) leading to
the mastoid antrum
2.The pyramid: a hollow conical
process containing the stapedius m.
3. The vertical part of the facial
canal ( for facial n.) med. To the
aditus.

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17. 17
Contents of middle ear
1. 3 ossicles : malleus, incus & stapes.
2. 2 muscles: stapedius & tensor
tympani.
3. 2 nerves: chorda tympani & tympanic
plexus.
4. Air.

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Figure showing malleus and its articular facets

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Figure showing incus and its articular facets

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Figure showing stapes bone

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Arterial supply
1. Ant. Tympanic a ( branch of maxillary a.)
2. Post. Tympanic a ( branch of post. Auric a.)
3. Superior tympanic a (branch of middle
meningeal a.)
4. Inf. tympanic a. (from asc. Pharyngeal a.)

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Lymphatic drainage
• The lymphatics of the middle ear & mastoid
antrum drain into parotid LNs & upper deep
cervical LNs.

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Middle ear functions

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30. ‫( ومه آَاجه اوك جسي األزض خاشعة فإذا أوزلىا علُها الماء اهحزت وزبث إن الرٌ‬
‫أحُاها لمحًُ المىجً اوه علً كل شٍء قدَس) – فصلت : 93.‬

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35. ‫{ لخلق السمىات واألزض اكبس مه خلق الىاس ولكه أكثس الىاس ال َعلمىن }‬
‫غافر : 75‬

36. 36
Complications of A.O.M.
• Def. spreading of infection beyond
the confines of pneumatized spaces
and the attendant mucosa of middle
ear

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38. 38
Aural
Complications
of A.O.M.
Aural complications :
1- mastoiditis .
2-labyrinthitis .
3- petrositis .
4- facial paralysis .

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Intracranial complications
1- extradural abscess or granulation
tissue .
2- dural venous sinus thrompophlebitis .
3- brain abcess .
4- otitic hydrocephalus .
5- subdural abscess .
6- meningitis .

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41. 41
Extradural complications:
. Extradural abscess
. Meningitis
. Sigmoid sinus thrombosis

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Intradural complications:
. Subdural abscess
. Brain abscess
. Otitic hydrocephalus

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Intratemporal complications:
. Facial palsy
. Labyrinthitis
. Petrositis
. Subperiosteal abscess
. Internal carotid artery aneurysm

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45. 45
Extratemporal complications :
• . Subclavian vein thrombosis
• . Luc's abscess
• . Citelli's abscess
• . Bezold's abscess

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Route of spread of infection from the ear:
1- extension through bone :demineralised during
acute infections,
cholesteatoma,
chronic disease of the ear..
2. Spread through venous channels:
Thrombophlebitis from the lateral sinus may
spread to the cerebellum, and from the superior
petrosal sinus may spread to the temproral lobe
of the brain.

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3. Spread through oval / round windows.
Spread may also occur through the
cochlear and vestibular aqueducts.
Certain areas may have dehiscent bone i.e.
bony covering of the jugular bulb,
dehiscent areas in the tegmen tympani,
and dehiscent suture lines of the temporal
bone.

48. 48
4. Spread may occur through trauma,
(accident, surgical) or by erosion due to
neoplasia.
5. Spread may occur through surgical
defects as caused by fenestration of the
oval window during stapedectomy
procedures.
6. Spread may occur directly into the brain
tissue through the peri arteriolar spaces of
Virchow Robin.

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Diagramatic representation showing the various routes of spread of infection from
the middle ear cavity.

50. 50
Factors that determine the spread
of infection:
I. Patient attributes: Patient's general
condition and
immunologic status
II. Bacterial attributes
the virulence of the infecting organism For
example acute infections caused by Strep.
pneumoniae type III, and H. Influenza type B
have immense potential to spread.

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Etiology and pathogenesis
1- streptococcus pneumoniae .
2- haemophilus influnzae
3- pseudomonas .

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Otoscopic examination

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Congested bulged eardrum ( impending rupture )

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Signs and symptoms of impending complications
1- persistent acute infection for two weeks .
2- recurrent symptoms of infection within two
weeks .
3- acute , fetid exacerbation of chronic infection .
4- fetid discharge during treatment .
5- H . Influnzae , type B , or anaerobes cultured
from the ear .
6- fever in the presence of a chronically perforated
tympanic membrane with or without
cholesteatoma .

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Severe earache Otoscopic examination

57. 57
Acute otitis media with bulged eardrum

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Left ear discharge in a case of complicated otitis media

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Aural swab for culture and sensetivity

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The most obvious complications
1- facial paralysis .
2- labyrinyhitis .
3- meningitis .
4- mastoiditis with subperiosteal abscess .

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clinical presentation
of complications of
acute otitis media

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Facial nerve paralysis

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Clinical presentation of facial paralysis
- If it occurs due to A.O.M. usually the
only complication .
- if it occurs due to cholesteatoma ,
horrizontal scc fistulae may exist .

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Acute otitis media complicated with right facial paralysis

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labyrinthitis

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Clinical presentation of labyrinthitis
1- ipsilateral SNHL .
2- Nystagmus ,
towards
contralateral side .
3- vertigo .

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Classifications of labyrinthitis
serous suppurative chronic
Cause toxins bacteria cholesteatoma
Hearing Preserve destroy all Preserved Hearing
some hearing
hearing
Associated Isolated meningitis ±SSC horizontal
Complications
Complica - (H) fistulae
tion ± dehiscence of
Fallopian canal
±facial paralysis

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meningitis

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Clinical presentation of meningitis
Causes
1- in A.O.M. , haematogenous dissemination .
2- In C.S.O.M. , dehiscence in dura .

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meningitis:
It is also known as Leptomeningitis.(only the
piamater and arachnoid are involved). This
is a major and serious complication of
middle ear infection. Nowadays, recovery is
usual provided early diagnosis and prompt
treatment is initiated.. Childhood otogenic
meningitis is commonly caused by acute
middle ear infections … it is a frequent
complication of chronic middle ear disease.

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meningitis
. Spread to the meninges may occur via any
of the dehicences in the bony barrier or
preformed channels or suppurative
labyrinthitis . Rarely rupture of brain
abscess into the subarachnoid space may
lead on to meningitis.

73. 73
causative organisms in meningitis:
acute infection :
H. Influenza type B, and Strep. pneumoniae
type III.
chronic ear diseases :
gram negative enteric organisms, proteus,
and psuedomonas. Anaerobes and
bacteriodes have also been reported.

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Pathogenèses of meningitis
The initial inflammatory response of the pia arachnoid
to infection is an outpouring of fluid into the
subarachnoid space, with a rise in CSF pressure. The
CSF becomes permeated with white blood cells and
rapidly multiplying bacteria. These bacteria feed on
glucose present in the CSF reducing its level in CSF a
characteristic finding in meningitis. Pus initially
accumulates in the basal cisterns, and more rarely in
the vertex. The free flow of CSF is impeded by the
exudate obstructing the ventricular foramina to cause
a non communicating hydrocephalus.

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Pathogenèses of meningitis
Obstruction to CSF in the subarachnoid spaces may
cause communicating hydrocephalus. Irritation of the
upper cervical nerve roots by the exudate cause neck
pain and neck stiffness which are the characteristic
features of this condition. Exudates around the exit
foramina of cranial nerves could cause nerve palsies
during the late stage of the disease. Spread of
infection through virchow robin spaces into the brain
substance may lead to the formation of brain abscess

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Clinical features of meningitis:
- headache and neck stiffness. At first the headache
localised to the side of the affected ear but later it
could become generalised and bursting in nature.
- malaise and pyrexia.
Initially neck stiffness shows resistance only to
flexion, but later full rigidity or retraction may
develop.
During early stages the patient may have mental
hyperactivity and restlessness.

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Clinical features of meningitis:
• Tendon reflexes becomes exaggerated during this
stage. Photophobia is another constant
presenting feature, and the patient may be
prompted to lie curled up away from the light.
Vomiting projectile in nature is another important
feature. As the condition worsens the symptoms
also become progressively severe. When neck
stiffness is marked the patient may manifest
poitive kernigs sign. The stiffness may become
more severe enough to cause opisthotonus.

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Diagnosis of meningitis
examination of CSF..
increased white cells
reduced glucose levels from 1.7-3 mmol/l to 0..
Chloride content may fall from 120 mmol/l to
80mmol/l.
Bacteria may also be isolated from the CSF.
Recently polymerase chain reaction have been used
to detect bacterial DNA from CSF.

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mastoiditis

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Clinical presentation of
mastoiditis
1- masked mastoiditis :
- mild discomfort in the ear with or without
mastoid tenderness .
- may exist with or without bone destruction
.

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Clinical presentation of
mastoiditis
2- obvious mastoiditis
( mastoiditis with subperiosteal abscess ) .
- mastoid tenderness .- pain.
- swelling .
- anteroinferior displacement of the ear .
- Spread to neck through incisura digastrics , ( Bezold
‘s abscess )
- spread under temporalis muscle through external
auditory canal ( Luc’ s abscess )

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Clinical presentation of
mastoiditis
N.B.
Mastoiditis may occur alone but often
result in a silent accumulation of
extradural abscess , or granulation tissue
.

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Acute mastoiditis in children and adult

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Acute otitis media with mastoiditis
+ Bulged ear drum

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Acute otitis media complicated with mastoiditis (left)

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Right coalescent mastoiditis

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Less obvious complications
1- subdural abscess .
2- otitic hydrocephalus .
3- petrositis .

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Subdural abscess

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Subdural abscess (Empyema):
• Spread of infection breaches the dura it
exposes the subdural space to the perils of
the infection. It may initially be associated
with Leptomeningitis, or if the infection is
contained as subdural effusions or subdural
abscess –
• extremely rare .
• devastatingly obvious by coma and focal
neurological signs .

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Pathogenesis of Subdural Abscess
• Spread of infection breaches the dura it exposes
the subdural space to the perils of the infection.
The granulation tissue which develops on the
inner side of the dura obliterates the subdural
space.
• Initially seropurulent effusion develops in the
subdural space, and eventually this becomes
frankly purulent.
• The spread of this effusion is limited by the
granulation tissue which attempts to obliterate
the subdural space.

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Pathogenesis Subdural Abscess
• The subdural pus tends to accumulate near the falx
cerebri, that too particularly where it joins the tentorium
cerebelli. Healing is always associated with fibrosis and
obliteration of the subdural space in the area where
granulation was present.
• The cortical veins in the adjacent area may become
involved by thrombophlebitis. This may also produce
multiple small abscess in the brain adjacent to the area of
subdural infection. One or numerous multiloculated
abscesses over the convex surface of the cerebral
hemispheres may be seen. Commonly Non haemolytic
streptococci have been implicated

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Clinical features of subdural abscess
headache and drowsiness.
Focal neurological symptoms like irritative fits and
paralysis
. Fits are usually of Jacksonian type, starting locally
and spreading to affect one side of the body this is
usually caused by cortical thrombophlebitis.
Paralysis may start with one upper or lower limb and
may gradually become hemiplegia.
If dominant lobe is involved aphasia develops.
Papilloedema is highly uncommon, and similarly
palsies involving individual cranial nerves are also
rare.

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Clinical features of subdural abscess
Meningism may accompany headache, distinguished
from meningitis by the presence of characteristic
neurological localising signs.
In children suspected of meningitis, subdural
empyema should be considered if there is no
response to treatment, or if motor seizures occur.

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Diagnosis of subdural abscess
•CT scan is diagnostic.
• M.R.I. is diagnostic ( easily )
•CSF examination :
•CSF pressure may be elevated,
•the sugar contents are normal ,
• the cultures are invariably sterile.
• In places where CT scan facilities are unavailable
exploratory burr holes may be made to clinch the
diagnosis
•.

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Otitic hydrocephalus

100. 100
Otitic hydrocephalus
Is one of the common complication of middle ear
infection. It is a syndrome of raised intracranial
pressure during or following middle ear infection.
This condition is also known as Pseudotumor
cerebri.
The onset may occur many weeks after acute otitis
media, or many years after the start of the chronic
middle ear disease.
usually associated with occlusive sigmoid sinus
thrombophlebitis and extradural abscess .

101. 101
Pathogenesis of otitic hydrocephalus
• The aetiology is unknown. The relationship of this
condition with that of lateral sinus thrombosis has
been documented.
• The inference is that obstruction of the lateral
sinus affects cerebral venous outflow, or the
extension of the thrombus into the superior
sagittal sinus impedes CSF resorption by
pacchionian bodies.

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Clinical presentation of otitic hydrocephalus
Characteristically present
with headache , some
degree of lethargy , severe
papilledema( blurred vision )
nausea ,vomiting , Lateral
rectus palsy on one or both
sides (stretching of the 6th
nerve due to increased
intracranial pressure ). C.T. is
diagnostic

103. 103
petrositis

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Clinical presentation of petrositis
- rarely ,if ever , present without mastoiditis .
- Intracranial complications are more frequent with
petrositis .
- Triad of Gradinigo :
- ear infection .
- ipsilateral retro – orbital pain .
- abducent palsy .

105. 105
Silent but exteremely serious complications
i. Masked mastoiditis
ii. Extradural abscess,
or granulation
tissue.
iii. Dural venous sinus
thrombophlebitis.
iv. Brain abscess.

106. 106
Extradural abscess

107. 107
Extradural abscess:
Is always associated with involvement of
dura mater by the spreading disease,
constituting pachymeningitis.
This is commonly preceded by loss of
bone, either through demineralisation in
acute infection or erosion by
cholesteatoma in chronic disease..

108. 108
Extradural abscess
If the cholesteatoma is non infected it may
simply expose the dura without any inflammatory
reaction.
If cholesteatoma is infected it is associated with
formation of granulation tissue over the dura.
Dura is tough and resists infection.
It attempts to wall off the infection, and
collection of pus occur between the dura and the
bone.
This is known as extradural abscess and is the
commonest of all intracranial complications.

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Figure showing extradural abscess

110. 110
Extradural abscess
A middle cranial fossa extradural mass may strip
the dura from bone on the inner surface of
squamous temporal bone.
Such an enlarging mass may cause increasing
intracranial tension, causing focal neurological
signs and papilloedema. Sometimes it could erode
the skull from inside to the exterior causing a
subperiosteal abscess i.e. the classic Pott's puffy
tumor. Rarely an extradural abscess may develop
medial to the arcuate eminence over the petrous
apex.

111. 111
Extradural abscess
This irritates the Gasserian ganglion of the
trigeminal nerve, and the 6th cranial nerve.
This produces the classic Gradenigo's
syndrome (includes facial pain, diplopia and
aural discharge). Posterior fossa extradural
abscess is limited by the attachments of the
dura laterally to the sigmoid sinus.
Posterior extension of this abscess around
the sigmoid sinus produces the perisinus
abscess. This could also extend to the neck
through the jugular vein

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Clinical feature of extradural abscess
Depends on the site of the abscess, its size,
duration and rate of development. In most
patients the symptoms are vague, and non
specific. Sometimes it could be a incidental
finding during mastoid surgery. The common
complaint of the patient being headache
accompanied by malaise. If the abscess
communicates with the middle ear the patient
may have interim relief following an episode
of aural discharge.

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Extradural abscess, or granulation tissue
• May occur in case of cholesteatoma.
• Often result from mastoiditis.
• Site:
1. In the middle fossa at the tegmen.
2. Along extraluminal surface of the lateral
wall of the sigmoid sinus.

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Lateral sinus thrombosis

115. 115
Dural venous sinus thrombophlebitis
• Begins as silent non-occluding phlebitis of the sinus
wall and induced mural thrombus, sigmoid sinus
thrombophlebitis.
• NB:
Sigmoid sinus thrombophlebitis & Extradural
granulation tissue should be thought
preoperatively and intraoperatively in every case
of suspected or operated mastoiditis

116. 116
Lateral sinus thrombosis:
Thrombophlebitis can develop in any of the veins
adjacent to the middle ear cavity. Of these the lateral
sinus, which comprise of the sigmoid and transverse
sinuses is the largest and most commonly
affected.
Formerly it was commonly associated with acute otitis
media in childhood; now it is commonly seen in patients
with chronic ear disease. In the preantibiotic era the
commonest infecting organism was beta hemolytic
streptococci. This organsim was known to cause
extensive destruction of red blood cells causing anaemia.
Now a days the infection is by a mixed flora

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Fig showing the various stages of lateral sinus thrombosis

118. 118
Pathogenèses of latéral sinus thrombosIs
Lateral sinus thrombosis is usually preceded by an
extradural perisinus abscess.
The mural thrombus partly fills the sinus.
The clot progressively expands and eventually occlude
the lumen.
The clot may later become organised, and partly broken
down and may even be softened by suppuration.
During this stage there is a release of infecting organism
and infected material into the circulation causing
bacteremia, septicemia and septic embolisation

119. 119
Pathogenesis of lateral sinus thrombosis
Extension to the confluence of the sinuses,
and to the superior sagittal sinus.
Invasion of the superior and inferior petrosal
sinuses may cause the infection to spread to
the cavernous sinus.
This spread into the brain substance accounts
for the very high association of with brain
abscess.
Downward progression of thrombus into and
through the internal jugular vein can reach the
subclavian vein.

120. 120
Clinical features of lateral sinus thrombosis :
.
The patients manifest with severe fever, wasting illness in
association with middle ear infection. The fever is high and
swinging in nature, when charted it gives an appearance of 'Picket
fence'. It is always associated with rigors.
The temperature rose rapidly from 39 - 40 degree Centigrade.
Headache is a common phenomenon, associated with neck pain.
The patient appear ematiated and anaemic.
When the clot extended down the internal jugular vein, it will be
accompanied by perivenous inflammation, with tenderness
along the course of the vein. This tenderness descended down
the neck along with the clot, and would be accompanied by
perivenous oedema or even suppuration of the jugular
lymph nodes.

121. 121
Clinical features cont. :
Perivenous inflammation around jugular foramen can
cause paralysis of the lower three cranial
nerves.
Raised intracranial pressure produce papilloedema
and visual loss.
Hydrocephalus could be an added complication if
the larger or the only lateral sinus is occluded by the
thrombus, or if the clot reaches the superior sagittal
sinus. Extension to the cavernous sinus can
occur via the superior petrosal sinus, and may cause
chemosis and proptosis of one eye.

122. 122
Clinical feature cont. :
If circular sinus is involved it could spread to the
other eye. The propagation of the infected emboli
may cause infiltrates in the lung fields, and may
also spread to joints and other subcutaneous
tissues.. These distant effects usually developed
very late in the disease, these could be the presenting
features if the disease is insiduous in onset. Masking
by antibiotics could be one of the causes. Patients
always feel ill, and persisting fever is usual.

123. 123
Clinical features cont. :
The patients may have ear ache, in association with
mastoid tenderness, and stiffness along the
sternomastoid muscle.
The presence of anaemia is rare now a days.
Papilloedema is still a common finding. Other
coexisting intracranial complications must be expected in
more than 50 percent of patients.

124. 124
Clinical features cont. :
.
Extension of infected clot along the internal jugular vein is
always accompanied by tenderness and oedema along the
course of the vein in the neck, and localised oedema over the
thrombosed internal jugular vein may still be seen.
One rare finding is the presence of pitting oedema over the
occipital region, well behind the mastoid process, caused by
clotting within a large mastoid emissary vein, this sign is known as
the Griesinger's sign.
Infact there is no single pathognomonic sign for lateral sinus
thrombosis and a high index of suspicion is a must in
diagnosing this condition

125. 125
Investigations of lateral sinus thrombosis :
A lumbar puncture must be performed, if
papilloedema does not suggest that raised intracranial
pressure may precipitate coning.
Examination of CSF
In uncomplicated lateral sinus thrombosis the white
blood count in the CSF will be low when the cause is
chronic middle ear disease, and somewhat raised in
acute otitis media.
The CSF pressure is usually normal.
The variations in the level of CSF proteins and sugar are
not useful.

126. 126
Investigations cont. :
Queckenstedt test: This is also known as Tobey - Ayer
test. This is recommended whenever lumbar puncture for
a possible intracranial infection is performed.
The test involves measurement of the CSF pressure and
observing its changes on compression of one or both
internal jugular veins by fingers on the neck. In normal
humans compression of each internal jugular vein in turn
is followed by an increase in CSF pressure, of about 50 -
100mm above the normal level. When the pressure over
the internal jugular vein is released then there is a fall in
the CSF pressure of the same magnitude

127. 127
CT scanning:
It may show filling defects within the sinus, and
increased density of fresh clots.
When contrast materials like Iothalamate (conray) is
used failure of opacification of the affected lateral sinus
may become evident.
The presence of septic thrombosis shows intense
inflammatory enhancement of the sinus walls and of the
adjacent dura. This enhancement of the walls, but not of
the contents of the sinus constitutes the empty triangle
or 'delta' sign.
It can also exclude accompanying complications like
brain abscess and subdural empyema.

128. 128
Angiography :
It helps to demonstrate the obstruction, its site and the
anatomical arrangement of the veins.
There is an
impending risk of displacing the infected thrombus
Arteriography:
Performed with radio opaque dye injected into the carotid
artery can show the venous outflow during the venous
phase. This can be clearly visualised in digital subtraction
angiography.
This technique involves precise superimposition of a
negative arteriogram on a positive film of bone structures.
This effectively cancels out the skeletal image thus clearly
revealing the vascular pattern.

129. 129
MRI:
Is sufficiently diagnostic hence angiography can
be avoided if MRI could be taken.
Established thrombus shows increased signal
intensity in both T1 and T2 weighted images.
MRI can also be used to show venous flow.
Gadolinum enhancement may show a delta sign
comparable with that seen on CT scans

130. 130
MR venogram that shows nonfilling of the
lateral sinus on the left side

131. 131
Brain abscess

132. 132
Otogenic brain abscess always develop in the
temporal lobe or the cerebellum of the same side
of the infected ear.
Temporal lobe abscess is twice as common as
cerebellar abscess.
In children nearly 25% of brain abscesses are
otogenic in nature, whereas in adults who are more
prone to chronic ear infections the percentage
rises to 50%.
The routes of spread of infection :
Retrograde thrombophlebitis of cerebral or
cerebellar veins from inflammed sigmoid sinus or
other adjacent dural sinuses ..
the commonest being the direct extension through
the eroded tegment plate.

133. 133
Although dura is highly resistant to
infection, local pachymeningitis may be
followed by thrombophlebitis penetrating
the cerebral cortex,
sometimes the infection could extent via
the Virchow - Robin spaces in to the
cerebral white matter.
Cerebellar abscess is usually preceded by
thrombosis of lateral sinus.
Abscess in the cerebellum may involve the
lateral lobe of the cerebellum, and it may
be adherent to the lateral sinus or to a
patch of dura underneath the Trautmann's
triangle.

134. 134

135. 135
Stages of formation of brain abscess:
Stage of cerebral oedema:
This is infact the first stage of brain abscess
formation. It starts with an area of cerebral oedema and
encephalitis. This oedema increases in size with
spreading encephalitis.
Walling off of infection by formation of capsule:
Brain attempts to wall off the infected area with the
formation of fibrous capsule. This formation of fibrous
tissue is dependent on microglial and blood vessel
mesodermal response to the inflammatory process.
This stage is highly variable. Normally it takes 2 to 3
weeks for this process to be completed.

136. 136
Stages of formation of brain abscess:
Liquefaction necrosis:
Infected brain within the capsule undergoes
liquefactive necrosis with eventual formation of pus.
Accumulation of pus cause enlargement of the
abscess.
Stage of rupture:
Enlargement of the abscess eventually leads to
rupture of the capsule containing the abscess and this
material finds its way into the cerebrospinal fluid as
shown in the above diagram.

137. 137
Pathological stages of Brain
abscess
1. Invasion( cerebritis):
Symptoms
Vague,mild headache, lethargy, malaise for several
days then resolve.
2. Localization : quiescence & latency.
Symptoms: totally silent for weeks
3. Enlargement :in which most abscesses manifest
with seizures or focal neurological signs.
4. Termination: the abscess catastrophically
rupture into the ventricle or subarachnoid space.

138. 138
Pathological stages of Brain
abscess
NB: brain abscess detected few weeks from onset
either clinically or radiologically.
It is prudent to look for brain abscess in case of
mastoiditis initially and again 3-4 weeks later

139. 139
The focal features of cerebellar abscess:
Weakness and muscle incoordination on the same side
of the lesion.
Ataxia causes the patient to fall towards the side of the
lesion.
Intention tremors which may become manifest by the
finger nose test.
Spontaneous nystagmus.
Dysdiadokinesis is also positive in these patients.

140. 140
Abscess in the cerebellum involves the lateral lobe of the cerebellum

141. 141
The focal features of
Cerebral (Temporo sphenoidal abscess):
Nominal aphasia, where the cerebral abscess in the dominant
hemisphere .
Visual field defects arise from the involvement of optic radiations.
Commonly there is quadrantic homonymous hemianopia, affecting
the upper part of the temporal visual fields
The visual field loss are on the side opposite to that of the lesion.
This can be assessed by confrontation method.
Upward development affects facial movements on the opposite
side, and then progressively paralysis of the upper and
lower limbs.
Paralysis first affects the leg , then arm and finally the face ,
if the expansion occur in inward direction .

142. 142

143. 143
Investigations for brain abscess :
CT scan and MRI scans with contrast media.
Reveal the position and size of the abscess,
the presence of localised encephalitis can be
distinguished from that of an encapsulated abscess.
Associated conditions such as subdural abscess, and
lateral sinus thrombosis can also be seen.
Lumbar puncture:
Is frought with danger because of the risk of coning.
Lumbar puncture must be performed in these patients
only in a neurosurgical unit where immediate
intervention is possible if coning occurs

144. 144
Diagnosis
of complications
in acute otitis media

145. 145
Diagnosis of complications
in acute otitis media
1. History & physical examination:
In history , look for symptoms :
i. Suggesting impending complications
ii. Retro-orbital or deep boring head pain
iii. Lethargy, headache or both, currently
and with the past 2 months.

146. 146
Diagnosis
In physical examination , look for signs :
i. Suggesting impending complications
ii. Diagnostic of obvious complications
iii. Catastrophic neurologic disease.
iv. Fuduscopic examination for papilledema.

147. 147
Early finding associated with
impending or established
intratemporal or itracranial
complications
1. Pain & fever ˃ 4 days despite appropriate ttt for AOM
2. Persisting fever & headache.
3. Radiographic evidence of a lytic lesion
4. Presence of anaerobes.
5. Excessive granulation tissue at surgery associated with
CSOM.
6. Chronic SOM with fever , headache , ear pain or vertigo.
7. Increasing otorrhea, meningeal signs , or impairment of
consciousness.
8. Headache with vomiting in patient with CSOM

148. 148
Diagnosis (cont.)
2. When a complication is
suspected , high resolution
C.T. for temporal bone and
associated brain with or
without contrast infusion is
indicated.
MRI is indicated if bone eroded
over sigmoid sinus or at the
tegmen.

149. 149

150. 150

151. 151
1. Normal transverse cross sectional anatomy of
the temporal bone at consecutive levels from
bottom to top.
A) Junction between the hypotympanun and the
mesotympanun at the level of the round window
niche (2). The tensor tympani muscle can be
seen extending towards the handle of the
malleus (6) and the tympanic membrane.
B) At the level of the basal turn of the cochlea
(3) forming the promontory which is part of the
medial wall of the mesotympanum.
C) At the level of the internal auditory meatus
(17) and the oval window (15). The
suprastructures of the stapes can be seen (8).
D) Epitympanon (20) housing the head of the
malleus (6) and the incus (7). The horizontal
portion of the facial nerve canal is passing
underneath the lateral semicircular canal.
E) Epitympanon (20) at the level of the lateral
semicircular canal (18) and the aditus ad antrum
(22).
F) Cross section of the two limbs of the superior
semicircular canal (18) at the level of the tegmen
tympani.

152. 152

153. 153
Advantages of MRI over C.T
1. It is more sensitive in detecting early cerebritis &
cerebral edema.
2. It is the most sensitive diagnostic tool in identifying the
site & size of epidural, subdural , and brain edema or
abscess.
3. It is more sensitive in detecting extraparenchymal
spread to subarachnoid space or ventricle
4. If mastoiditis or sigmoid sinus phlebitis is surgically
proven, repeat MRI is indicated 3-4 weeks post
operatively to detect subsequent development of an
occult brain abscess.

154. 154
diagnosis
• Angiography: is a definitive investigation of lateral sinus
thrombosis. It helps to demonstrate the obstruction, its
site and the anatomical arrangement of the veins. There is
an impending risk of displacing the infected thrombus.
• Arteriography: performed with radio opaque dye
injected into the carotid artery can show the venous
outflow during the venous phase. This can be clearly
visualised in digital subtraction angiography. This
technique involves precise superimposition of a negative
arteriogram on a positive film of bone structures. This
effectively cancels out the skeletal image thus clearly
revealing the vascular pattern.

155. 155
Apex petrositis in a 50-year-old woman with Gradenigo syndrome at
clinical evaluation. (a) Axial T1-weighted MR image shows an irregular
lesion at the tip of the petrous apex (arrow). (b) Contrast-enhanced
axial T1-weighted MR image shows right-sided apex petrositis as an
enhancing lesion along the courses of cranial nerves V and VI (arrow).

156. 156
Diagnosis (cont.)
3. Funduscopic examination: in case of suspected
meningitis or otitic hydrocephalus. or intracranial
abscess.
4. Lumber puncutre: in case of suspected meningitis or
otitic hydrocephalus.
• Finding in meningitis: high protein, low glucose level,
presence of micro-organisms on Gram’s stain.
• Finding in otitic hydrocephalus: normal protein &
glucose levels, -ve gram’s stain & elevated opening
pressure.
5. Surgical exploration.

157. 157
Treatment
of complications of
acute otitis media

158. 158
Treatment of complications
of acute otitis media
For all complications:
i. Admission
ii. I.V. antibiotics
iii. Surgical intervention.

159. 159
I. Acute coalescent mastoiditis and
masked mastoiditis with or without
subperiosteal abscess:
Wide myringotomy, complete canal wall up
mastoidectomy, and wide facial recess to
maintain the aditus & antrum patent.

160. 160
II. Petrositis :
Total resection of tympanic membrane ossicles
insitu with resection of posterosuperior canal
wall (Modified radical mastoidectomy).
Later on reconstruction of the tympanic
membrane in healed ear.
NB:If persistent infection: middle fossa app.
combined with lat. app.

161. 161
III. Chronic mastoiditis:
Canal wall up or canal wall down procedure.
reconstruction of the middle ear at the same
setting.
NB: during mastoidectomy for suppurative
disease, inspection of the dura of the tegmen,
sigmoid sinus, and facial nerve through thin
bone is crucial. To avoid leaving unrecognized
and untreated granulation tissue.

162. 162
IV. Labyrinthitis (acute) :Myringotomy.
V. Labyrinthitis in C.S.O.M with or without
cholesteatoma:
Tympanoplasty and mastoidectomy.
If fistula is in the cochlea, better to leave the
chlesteatoma matrix on the fistula, remove it after
healing.
If fistila in semicircular canals, the chlesteatoma matrix
carefully removed and fascia placed over the fistula.
But if matrix attache to membranous labyrinth,
matrix left and removed later.
As suppurative labyrinthitis may soon associated with
meningitis, hospitalization and IV antibiotics
continued until infection eradicated

163. 163
VI. Facial paralysis :
Myringotomy.(in acute
infection).
Facial paralysis in chronic or
subacute infection:
Mastoidectomy to eradicate
disease & to explore the
fallopian canal for invasive
granuloma.

164. 164

165. 165
Myringotomy with ventilation tube
insertion

166. 166
VIII.Extradural granulation tissue:
wide exposure of abnormal dura,
careful attempt to bluntly remove excess
granulation tissue.

167. 167
Extradural abscess
Surgery must be done as early as possible.
Drainage into the mastoid. If abscess is
encountered, canal wall up should be taken
down so that complete drainage is ensured.
Granulation tissue over the dura should not
be disturbed because it could breach the
only defence and the infection could spread
to the brain.

168. 168

169. 169
IX.
Dural venous thrombophlebitis:
 Complete mastoidectomy.
 I.V antibiotic
 Reduce I.C pressure by : hyperventilation,
therapeutic lumber puncture, mannitol &
dexamethazone.
 Careful opening of sinus to explore for intraluminal
abscess, drained into mastoid . or intraluminal
fibrotic, non abscessing mural thrombus.
 If bleeding occur with sinus opening, can be
controlled with extraluminal piece of surgical , a
piece of fascia may be placed lateral to surgical.

170. 170
IX. Dural venous thrombophlebitis ( contin.):
 Internal jugular vein ligation: if continuing sepsis,
extension of thrombus, pulmonary complication
with contiunous spiking fever.
 Anticoagulants & thrombolytics: if associated with
otitic hydrocephalus.
 Direct intrasinus thrombolytic ttt with urokinase and
streptokinase: in case with progressive neurologic
deterioration with evolution of thrombus,
transvenosus.

171. 171
X. Brain abscess:
 ttt under the guidance of neurosurgery.
 Empiric ttt with penicillin or β-lactam antibiotic,
chloramphenicol, and metronidazole and IV
dexamethazone.
 Mannitol ,hyperventilation (to decrease I.C.P)
 Burr hole aspiration and stereostatic drainage.
 Serial stereostatic aspiration (procedure of choice)
 Concurrent craniotomy and mastoidectomy. Avoid
reinfection , results in a single , shorter hospital stay.

172. 172
Repeated aspiration are
preferred to complete excision
1. Multiple abscesses in deep or dominant
location.
2. With concomitant meningitis with early
response to antibiotics
3. Abscesses <3cm

173. 173
XI. Otitic hydrocaphalus:
 ttt mastoiditis, extradural granulation & sigmoid sinus
thrombophlebitis.
 Most cases resolve spontaneously in months
 ttt with acetzolamide and furosemide or systemic
steroid.
 Lumoperitoneal shunt: for patient with deterioration
of vision or for patient with disabling pulsatile tinnitus.
 Ophthalmologist follow the patient’s vision.
 Long term care of intracranial hypertension by
neurologist.
NB: Blindness or brain herniation are serious concerns.

174. 174
XII.Subdural abscess:
 ttt under the guidance of neurosurgery.
 ttt : I.V antibiotics, anticonvulsants and steroids.
 Neurosurgical drainage with mastoidectomy may
be done together or sequentially.
 Surgical control of mastoiditis, extradural
granulation or abscess , and sigmoid sinus
thrombophlebitis is crucial for recovery.

175. 175
XIII.Meningitis :
 Appropriate I.V antibiotics and dexametasone.
 Myringotomy.
NB: meningitis from CSOM (pus directly from ear into
subarachnoid space)
 Radical mastoidectomy with exploration of all
dural surfaces directly or through thin bone is
necessary. Repair dural defect with fascia placed
intradurally and extradurally.

176. ‫النساء :‬ ‫{ .... وعلمك ما لم جكه جعلم وكان فضل هللا علُك عظُما }‬
‫311‬

177. ‫اجلاثية : 63‬ ‫{فلله احلمد رب السموات ورب األرض رب العاملني}‬

178. 178
THANK YOU
Dr, IBRAHIM HABIB BARAKAT,M.D.
( Otorhinolaryngology )
https://www.facebook.com/Dr.Ibrahim.Barakat
salamatuall@hotmail.com
salamatuall@yahoo.com