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 ofthe middle ear cavity

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

Formed by thin plate of bone called « tegmen tympani »It separates the middle ear cavity from the temporal lobe in the middle cranial fossa

Roof (tegmentalwall)

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.

The floor

Formed mainly by the ear drumLateral wall

Contains the following structures (arranged from above downwards):1. The opening for the canal of tensor tympani m2. The opening for Eustachian tube.3. A plate of bone separating the middle ear from the I.C.A in the carotid

canal.

Anterior wall

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Surfaces of the middle ear

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 internalear.

3. Rounded window: lies below & behind the promontry & is closed by 2ry tympanic membrane.

4. The horizontal part of facial canal :archingabove the promontary & oval window.

Medial wall

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Surfaces of the middle ear

Contains the following structures (arranged from above downwards):

1.The aditus ( opening ) leading to the mastoid antrum

2.The pyramid: a hollow conicalprocess containing the stapedius m.

3. The vertical part of the facial canal ( for facial n.) med. To the aditus.

Posteriorwall

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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

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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ومه آاجه اوك جسي األزض خاشعة فإذا أوزلىا علها الماء اهحزت وزبث إن الر ) . 39: فصلت –( أحاها لمح المىج اوه عل كل شء قدس

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{ لخلق السمىات واألزض اكبس مه خلق الىاس ولكه أكثس الىاس ال علمىن } 57: غافر

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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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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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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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.

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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.

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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.

Etiology and pathogenesis1- streptococcus pneumoniae .

2- haemophilus influnzae

3- pseudomonas .

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Otoscopic examination

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Congested bulged eardrum ( impending rupture )

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

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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

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

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

Clinical presentation of labyrinthitis

1- ipsilateral SNHL .

2- Nystagmus , towards contralateral side .

3- vertigo .

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Classifications of labyrinthitis

chronicsuppurativeserous

cholesteatomabacteria toxins Cause

Preserved Hearingdestroy allhearing

Preserve some hearing

Hearing

±SSC horizontal(H) fistulae± dehiscence ofFallopian canal±facial paralysis

meningitisIsolatedComplica -tion

AssociatedComplications

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meningitis

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.

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: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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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.

Pathogenèses of meningitis

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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

Pathogenèses of meningitis

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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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.

Diagnosis of meningitis

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mastoiditis

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

Acute otitis media with mastoiditis

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+ Bulged ear drum

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Acute otitis media complicated with mastoiditis (left)

Right coalescent mastoiditis

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Less obvious complications

1- subdural abscess .

2- otitic hydrocephalus .

3- petrositis .

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Subdural abscess

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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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.

Clinical features of subdural abscess

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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.

Clinical features of subdural abscess

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

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 .

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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

.

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petrositis

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 .

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Silent but exteremely serious complications

i. Masked mastoiditis

ii. Extradural abscess, or granulation tissue.

iii. Dural venous sinus thrombophlebitis.

iv. Brain abscess.

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Extradural abscess

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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..

Extradural abscess:

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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.

Extradural abscess

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Figure showing extradural abscess

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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.

Extradural abscess

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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

Extradural abscess

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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.

Clinical feature of extradural abscess

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

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

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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

Lateral sinus thrombosis:

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Fig showing the various stages of lateral sinus thrombosis

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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

Pathogenèses of latéral sinus thrombosIs

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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.

Pathogenesis of lateral sinus thrombosis

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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.

Clinical features of lateral sinus thrombosis :

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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.

Clinical features cont. :

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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.

Clinical feature cont. :

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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.

Clinical features cont. :

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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

Clinical features cont. :

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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.

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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

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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.

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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.

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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

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

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Brain abscess

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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.

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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.

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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.

Stages of formation of brain abscess:

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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.

Stages of formation of brain abscess:

Pathological stages of Brain abscess

1. Invasion( cerebritis): SymptomsVague,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.

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Pathological stages of Brain abscess

NB: brain abscess detected few weeks from onseteither clinically or radiologically.

It is prudent to look for brain abscess in case of mastoiditis initially and again 3-4 weeks later

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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.

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Abscess in the cerebellum involves the lateral lobe of the cerebellum

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 .

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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

Investigations for brain abscess :

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Diagnosisof complications

in acute otitis media

Diagnosis of complicationsin acute otitis media

1. History & physical examination:

In history , look for symptoms :

i. Suggesting impending complicationsii. Retro-orbital or deep boring head pain

iii. Lethargy, headache or both, currently and with the past 2 months.

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Diagnosis

In physical examination , look for signs :

i. Suggesting impending complicationsii. Diagnostic of obvious complicationsiii. Catastrophic neurologic disease.iv. Fuduscopic examination for papilledema.

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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

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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.

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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.

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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.

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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.

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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).

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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.

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Treatment of complications of acute otitis media

Treatment of complications of acute otitis media

For all complications:

i. Admission

ii. I.V. antibiotics

iii. Surgical intervention.

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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.

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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.

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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.

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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

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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.

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Myringotomy with ventilation tube insertion

VIII.Extradural granulation tissue:

wide exposure of abnormal dura,

careful attempt to bluntly remove excess granulation tissue.

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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.

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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.

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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.

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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.

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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

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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.

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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.

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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.

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: النساء { وعلمك ما لم جكه جعلم وكان فضل هللا علك عظما .... }

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36: اجلاثية {فلله احلمد رب السموات ورب األرض رب العاملني}

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THANK YOU Dr, IBRAHIM HABIB BARAKAT,M.D.

( Otorhinolaryngology )

https://www.facebook.com/Dr.Ibrahim.Barakatsalamatuall@hotmail.comsalamatuall@yahoo.com