The complications of otitis

media

Complications
Complications within the
within the cranium temporal bone

Extradural Intradural
complications :complications mastoiditis.
Extradural abscess Subdural absceSS. Labyrinthitis.
Meningitis Brain abscess. Petrositis.
sigmoid sinus Otitic. Facial palsy.
thrombosis hydrocephalus
Diagramatic representation of intracranial complications
media
Route of spread of infection from the ear:

1. Extension through bone

2. Spread through venous channels
3. Spread through normal anatomical pathways
4.Spread may occur through non anatomical bony defects
5.Spread may occur through surgical defects
Factors that determine the spread of
infection:
Patient's general condition and immunologic
status .
The virulence of the infecting organism.
Adequacy / Inadequacy of treatment of the
middle ear condition.
Pneumatization of mastiod air cells.
 Intra cranial complication
A)Extra dural complication:
1)Extra dural abscess:
Def: it’s accumulation of pus against dura
matter ,It’s the commonest of all intracranial
complications.
 A)Extra dural complication:
1)Extra dural abscess
Pathogenesis
-This is commonly preceded by loss of bone,
either through demineralisation in acute
infection or erosion by cholesteatoma in
chronic disease.
A) If cholesteatoma is non infected
expose dura without inflammation.
B) If cholesteatoma is infected form
granulation tissue over dura
 A)Extra dural complication:
1)Extra dural abscess
Clinical features:
1- Headache on the side of otitis media.
2-pulsating discharge.
3-fever.
 A)Extra dural complication
1)Extra dural abscess
Management:
a)Diagnosis:
CT SCAN
b)Treatment:
mastoidectomy and drainge of abcess.
 A)Extra dural complications
2)Meningitis :
Pathology:
Csf characteristic:
1- contains WBCs.
2-Contains rapidly
multiplying bacteria.
3-Decreases glucose level .
 A)Extra dural complication
2)Meningitis :
Clinical features
-General symptoms
-Signs due to meningeal irritation:
1- Neck stiffness
 A)Extra dural complication
2)Meningitis :
2- poitive kernigs sign
 2)Meningitis :
3-Brudzinski's sign
 A)Extra dural complication
2)Meningitis :
Management:
a)Diagnosis:
lumbar puncture
b)Treatment:
systemic antibiotics, Penicillin, Streptomycin ,
Chloramphenicol, Ceftrioxine
 A)Extra dural complication
3)Lateral sinus thrombosis:
Pathogenesis:
 A)Extra dural complication
3)Lateral sinus thrombosis:
Clinical features:
Signs of blood invasion
Positive greissinger’s sign
Raised intracranial pressure:
Papilloedema and visual loss.
Hydrocephalus

Tenderness and oedema along the course of

the vein in the neck
 A)Extra dural complication
3)Lateral sinus thrombosis:
Investigations:
1)-A lumbar puncture
2)Queckenstedt test( Tobey - Ayer test)
 A)Extra dural complication
3)Lateral sinus thrombosis:
Management:
a)Diagnosis:
CSF show:
1) increased white cells and reduced glucose levels.
2) Increase bacteria content.
 A)Extra dural complication
b)Treatment:
Medical:
systemic antibiotics
- Streptomycin.
-Chloramphenicol
Surgical:
modified radical mastoidectomy
 B)Intra dural complication:
1)Brain abcess
Stages of formation :
1-stage of cerebral
oedema.
2-stage of Liquefaction
necrosis.
3-Stage of rupture.
4-Stage of chronic
abcess.
 B)Intra dural complication:
1)Brain abcess

Clinical features:
1-Stage of invasion:-
headache, fever, malaise and vomiting.
2-latent stage:-
asymptomatic.
3-stage of expansion:
signs of increased intracranial pressure:
B)Intra dural complication:
1)Brain abcess
localizing signs

1)Cerebral 2)Cerebellar
abscess

-Hemiplegia
or
- nominal hemiparesis.
aphasia - weakness
- Visual field and muscle
defects incoordinatio
n
- Ataxia
Intention tremors
Spontaneous nystagmus.
Dysdiadokinesis
4-Last stage:
Unless brain abcess treated : it ends by death due to
-coning of brain steam.
-rupture of abcess.
 B)Intra dural complication:
1)Brain abcess
Management:
a)Investigations:
CT scan and MRI scans
Lumbar puncture
B)TREATMENT:
large doses of antibiotics.
-Measures to decrease intracranial pressures.
Incision and drainge.
-mastoidectomy
 B)Intra dural complication:
2)Otitic hydrocephalus:
Def: It is a syndrome of raised intracranial
pressure during or following middle ear
infection.
Pathogenesis:
Obstruction of the lateral sinus affects
cerebral venous outflow, or the extension of
the thrombus into the superior sagittal sinus
impedes CSF resorption by pacch ionian
bodies.
 B)Intra dural complication:
2)Otitic hydrocephalus:
Clinical features:
symptoms : Signs:
1. headache 1)papillodem
2. drowsiness a
2)Lateral
3. blurred vision
4. nausea rectus palsy.
5. vomiting
6. diplopia
 B)Intra dural complication:
2)Otitic hydrocephalus:
Management:
a)Diagnosis:
CT scan is diagnostic.
b)Treatment:
1) Reduce CSF pressure
2)Treat the ear infection
 Intratemporal complications
1)Acute mastioditis
Def: acute infection of the mastoid antrum
and air cells with destruction of the
intercellular bony septa.
Pathology:
 Intratemporal complications
1)Acute mastioditis
 Outer table mastoid abcess
 Mastiod tip bezold's abcess.
 Roor of zygoma zygomatic abcess.
 Lateral sinus lateral sinus thrombosis.
 Petrous apex ptreositis.
 Intratemporal complications
1)Acute mastioditis
Clinical picture:
Symptoms :
1-fever
2- otalgia
3- mucopurulent discharge
Signs:
1-Profuse mucopurulent discharge
2-Tenderness and redness over the mastoid.
3-Oedema of the posterior superior wall of
 Intratemporal complications
1)Acute mastioditis

Mangement:
a)Investigation:
haziness in
X-ray will show mastioditis.

abcess cavity in
mastoid abcess.
 Intratemporal complications
1)Acute mastioditis
b)Treatment:
-Medical treatment :
1-Cleaning ear discharge
2-Antibiotic.
3-Antipyritic
-Surgical treatment:
Cortical mastiodictomy
Insertion of tympanostomy tube to drain pus.
 Intratemporal complications
2)Petrositis:
Def: It's inflammation of the petrous air
cells with destruction of the intercellular
bony septae.
Pathology:
Accumulation of pus under pressure in the
petrous air cells will lead to pressure
necrosis of the inter cellular bony septa.
 Intratemporal complications
2)Petrositis:
Clinical picture:
It's characterized by triad (gradenigo's sign):
1- Otorrhea
2-Retrobulber pain
3- Diplopia
Treatment:
Mastoidectomy
 Intratemporal complications
3)Labyrinthitis:

Def: is an inflammation of the

membranous labyrinth which may be:
1)Toxic
2)Bacterial
 Intratemporal complications
3)Labyrinthitis:
Pathology:
1)Serous stage
2)Suppurative stage: It's irreversible
stage.
3)fibrous stage
4)Osseous stage
 Intratemporal complications
3)Labyrinthitis:
clinical picture
(1)-serous stage:
(2)-Suppurtive stage: the same
manifestation but become more severer.
(3)-Fibrous stage
(4)Osseous stage: there's difficulty in
cochlear implantation
 Intratemporal complications
3)Labyrinthitis:
Treatment:
1-Antibiotic
2-Surgical :
-Myringotomy in AOM.
-Mastiodictomy in COM.
3-Drainge of labyrinth
 Intratemporal complications
4) Facial palsy:
It occur due to facial canal
dehiscent leading to lower motor
neuron facial.
40
 It is formed by two
roots

Motor Nervus
intermedi
us

1. Sensory
afferents
2. Preganglionic
parasympatheti
It emerges from the brainstem between the pons
and the medulla. c
41
Divided
into 6
segment
s

42
 Facial nerve

Horizontal segment Mastoid segment

 facial nerve in meddle ear
Tympanic or horizontal segment

♦It extends from the geniculate ganglion to

the horizontal semicircular canal and is 8-11
mm in length.
 ♥The nerve passes behind the
cochlear form process and the
♥The nerve
tensor tympani.
lies against the
medial wall of
the vacuum
tympani,
above and
posterior to
the oval
window.
nerve sheath. ♦The
fallopian canal has been
reported to be dehiscent
in the area of the oval
window in 25-55% of
postmortem specimens.
Always anticipate finding
a dehiscent or prolapsed
facial nerve in its
tympanic segment,
especially in patients with
congenital ear
deformities.
 N.B
♦The most important

landmarks for
identifying the facial
nerve in the mastoid
are the horizontal
semicircular canal,
the fossa incudis,
and the digastric
ridge.
 .Mastoid segment

♦The second genu marks the beginning of the

mastoid segment. The nerve continues
vertically down the anterior wall of the mastoid
process to the stylomastoid foramen.
♦The mastoid segment is the
longest part of the intratemporal
course of the facial nerve,
approximately
10-14 mm long.
The 3 branches that exit from the mastoid
segment of the facial nerve ar
• (1) the nerve to the stapedius
muscle.
(2)nerve
the the chorda
from thetympani
auricular(nerve
3)
. branch of the vagus
 N.B
• auricular branch of the vagus nerve
arises from the jugular foramen and
joins the facial nerve just distal to the
point at which the nerve to the
stapedius muscle arises. Pain fibers
to the posterior auditory canal may
be carried with this nerve .
• Structure of facial nerve
• The axons are surrounded by myelin,
produced by the Schwann cells
surrounding the axons.
• Three membranes comprise the nerve
sheath.
• a-The epineurium is the outer covering.
• b-The perineurium is the next more inner
layer.
• C- endoneurium surrounds the individual
nerve fibers.
• It is a weakness or paralysis of the
nerve that control facial expression on
one side of the face .
 N.B
• Facial paralysis is most often caused
by a virus infection of the facial nerve.
However, other conditions such as
tumors, other infections,
• trauma, among others.
• The condition is more
• frequent in diabetics
• and pregnant women. 
 Causes of facial
nerve lesion

Supranuclear and Infranuclear

nuclear lesion lesions
 Causes of
Infranuclear
lesions…….???
 1-Trauma:-
• physical, especially fracturesof the
temporal bone, may also cause acute
facial nerve paralysis.
;-Transverse fractures
). present the highest likelihood of facial paralysis (40-50% ♦

Patients may also present♦

with hemotympanum ,
sensory deafness, and
vertigo – the latter two
symptoms due to damage
to vestibulocochlear nerve
.and the inner ear
• Longitudinal fracture
• present a lower likelihood of
paralysis (20%).
• ♥Patients may present with
• hematorrhea , tympanic
membrane tear, fracture of
external auditory canal, and
:-conductive
Diagnosis hearing loss
) Computed tomography (CT
) nerve conduction studies (ENoG
• Management:-
• ♦If nerve conduction studies show a large
(>90%) change in nerve conduction, the
nerve should be decompressed.
• ♦The facial paralysis can follow immediately
the trauma due to direct damage to the
facial nerve, in such cases a surgical
treatment may be attempted.
• ♦In other cases the facial paralysis can
occur a long time after the trauma due to
oedema and inflammation.
• 2-Herpes zoster oticus:
• -(Ramsay Hunt syndrome (RHS)
type 2)
• It is a disorder that is caused by the
reactivation of pre-existing
• Herpes zoster virus in
• a nerve cell bundle in the head
• (the geniculate ganglion).
• Symptoms and signs:-
• ♦ acute facial nerve paralysis, (pain in the ear,
• taste loss in the front two-thirds of the tongue, dry
mouth and eyes),
• ♦eruption of a erythematous vesicular rash in the
ear canal, the tongue, and/or hard palate.
• ♦ It may also affect vestibulocochlear nerve and
patients may also suffer from tinnitus, hearing loss,
and vertigo.
• Prognosis:-
• ♦complete recovery can be achieved in 75% of
patients if treatment with prednisone and
acyclovir is started within the first 3 days of
onset of facial paralysis.
♦ Chances of complete recovery decrease as
treatment is delayed, may lead to complete loss
of response to facial nerve stimulation.

• Treatment apparently has no effect on the

recovery of hearing loss.
• Diazepam is sometimes used to treat the vertigo.
N.B
 3-Acute and chronic otitis
media:-
• Facial palsy can present as
complication of acute suppurative otitis
media, otitis media with effusion,
chronic otitis media, and mastoiditis.
N.B

♥ infection involving the

fallopian canal can lead
to inflammation and
neural edema.
♥Immediate treatment should be directed toward
eradicating the infection.
♥myringotomy is performed promptly to drain the
middle ear space.
♥ antibiotic therapy against the offending organism.

♦ The incidence of facial palsy in acute otitis media is

approximately 1:20,000 cases.
☻Most cases are seen in children due to the greater
incidence of acute otitis media in them.

♦The prognosis is excellent. Recovery of facial

function begins rapidly in conjunction with
resolution of infection.
♥Operative management is limited to myrigotomy and
tube.
• ☺ Facial palsy in association with chronic
otitis media or cholesteatoma carries
amore ominous prognosis.
• ☺The development of paralysis is often
more insidious.
• ☺ Aural toilet and antibiotic
• are initiated promptly.
• If the tympanic
• membrane is intact,
• myringotomy
• is performed.
• 4- Neurosarcoidosis:-
• - sometimes bilateral, itself a rare condition.
• 5-Tumors:-
• A tumor compressing the facial nerve anywhere
along its complex pathway can result in facial
paralysis. Common culprits are facial neuromas ,
congenital cholesteatomas, hemangiomas,
acoustic neuromas,
• parotid gland neoplasms,
• or metastases
• of other tumors
• Diagnosis:-
• 1-Computed tomography (CT) or
magnetic resonance (MR) .
•Head
2-Physical:-
and neck♥
examination
•Tests for facial innervation include the following:
☻Forehead wrinkling (frontalis muscle)
☻ Eye closure (orbicularis oculi muscle)
☻ Wide smile
☻Whistling
☻Blowing
 N.B

• Clinical diagnosis is based on 3

steps, identification of the
affected site, underlying etiology
(trauma, infectious, neoplastic),
• and finally, clinical staging
• (eg, with use of the
House-Brackmann scale).
 House-Brackmann Classification of Facial Function
Grade Description Characteristics
I Normal Normal facial function in all
areas
II Mild dysfunction Slight weakness noticeable on
close inspection; may have
very slight synkinesis
III Moderate Obvious, but not disfiguring,
dysfunction difference between 2 sides;
noticeable, but not severe,
synkinesis, contracture, or
hemifacial spasm; complete
eye closure with effort
IV Moderately Obvious weakness or
severe disfiguring asymmetry; normal
dysfunction symmetry and tone at rest;
incomplete eye closure
Treatment:-
• ♦Treatment of the facial paralysis depends on
the cause of the facial paralysis.
• ♦In cases of infections, antibiotics are
prescribed and surgery may be necessary.
• ♦In other cases, steroid medication
(prednisone) is prescribed in combination
with an anti-viral medication.
• In cases of tumor or paralysis resulting from
resection of tumors of head and neck, the
treatment usually consists of one or more of
various facial reanimation procedures.
• ♥A critical element of the treatment of facial
paralysis is the care of the eye.
 facial nerve
repair

Nerve
Primary facial Cable nerve
substitution
nerve repair grafting
techniques

Hypoglossal-♦
facial
anastomosis
♦Cross-face grafting