This document discusses various complications that can arise from otitis media infections, including both intracranial and extracranial complications. It classifies complications into two broad groups: intracranial complications such as extradural abscess, subdural abscess, brain abscess, meningitis, sigmoid sinus thrombosis, and otic hydrocephalus; and extracranial complications including mastoiditis, otitis externa, facial nerve palsy, petrositis, labyrinthitis, internal jugular vein thrombosis, and adhesive otitis media. It provides details on symptoms, causes, and treatments for several of these complications.

1. Prof. Dr. Ausaf Ahmed Khan
MBBS. DLO. FCPS. FRCS(Glasg)
Member IWGEES (International Working Group
of Endoscopic Ear Surgery)
Head of ENT / Head and Neck Surgery
Hamdard College of Medicine & Dentistry
Hamdard University. Karachi, Pakistan

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Introduction
• Complications of suppurative otitis media arise
when the infection spreads from the ME cleft
to structures from which it is normally
separated by bone.
• Before antibiotics regular usage, complications were
more common with AOM
• Now they are more common with CSOM.
• The overall incidence of complications has fallen now
because of regular antibiotics usage.

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Intracranial
complications
– Extradural abscess
– Subdural abscess
– Brain abscess
– Meningitis, Encephalitis
– Sigmoid sinus thrombosis
– Otic hydrocephalus
Extracranial
complications
– Mastoidits
– Otitis externa
– Facial N. palsy
– Petrositis
– Labyrinthitis
– I.J.V. thrombosis
– Adhesive Otitis Media
Complications can be broadly
classified into 2 groups;

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Infection may spread from the ME & mastoid
antrum through these routes;
1. By extension through bone that has been
demineralized during acute infection.
2. Through normal anatomic pathways; e.g. round &
oval window, vestibular & cochlear aqueducts,
dehiscence of the jugular bulb or tegmen tympani.
3. Through non-anatomical bony defects; e.g.
accidental or surgical or by neoplastic erosion
Routes of spread

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Mural thrombus Occluding thrombus
Inflammation of
outer dural wall Propagating thrombus
Central breakdown
Abscess formation

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• In chronic infections  disease spread
slowly and many of its infections are caused
by progressive erosion of the bone.
• In acute infections  complications develop
earlier through thrombo-phlebitic mechanism
and the anatomical available pathways.
Mechanism of spread

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The propensity for spread of infections and the
development of complications depend on;
1. Patient factors; age, immunity, intercurrent
chronic disease e.g. DM, leukemia.
2. Bacterial factors; virulence, susceptibility to
chemotherapeutic elimination
3. Efficacy of treatment of the underlying
middle ear disease.

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Extracranial
Complications
1. Mastoiditis
2. Otitis externa
3. Facial N. palsy
4. Petrositis
5. Labyrinthitis
6. I.J.V. thrombosis
7. Adhesive Otitis Media

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M A S T O I D I T I S
• It is the inflammation of the bony septa of
the mastoid bone
• It occurs when the infection extends beyond
the lining mucous membrane of the mastoid
air cells to involve underlying bone.
 Some degree of mastoid cells inflammation is
commonly associated with all Middle Ear infections.
• Mastoiditis may be acute or chronic,,,,
– Acute ; usually associated with ASOM.
– Chronic ; associated with CSOM.

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Acute Mastoiditis
• In Ac. mastoiditis, there is severe
inflammation and pus is present in the
mastoid air cells under the periosteum.
• Continued infection in absence of proper
therapy causes hyperemia and thickening of
the mucoperiostium, impeding the drainage
of secretion and stasis.

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Prognosis of Acute Mastoiditis
ASOM
Subclinical mastoid infection
Mastoid empyema
Acute coalescent mastoiditis
Intratemporal complications
Intracranial complications
Subperiosteal abscess
Petrositis

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TM
Mstd
Brn

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Acute Mastoiditis
• Hyperemic decalcification of the mastoid air
cells  resorption of bone & loss of
trabeculation formation of an empyema
because small air cells coalesce into large
cavities
• If this process is extensive enough it reaches
the surface of the bone to form sub-periosteal
abscess.
• These abscesses, if left untreated may spread
in several directions . . . . .
•

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Acute Mastoiditis
• Spread laterally  destroy
periosteum & overlying skin 
form postaural abscess/ fistula
with discharge.
Spread of Mastoid abscess - 1

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Acute Mastoiditis
• Extends anteriorly
towards the EAC
 sagging of the
posterior meatal
wall.
Spread of Mastoid abscess - 2

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Acute Mastoiditis
• May erode the mastoid tip discharge
pus in sheath of Ant. belly of digastric
(citelli’s abscess).
Spread of Mastoid abscess - 3
Citelli’s abscess
Bezold’s abscess
Mstd
Post -
auricular
abscess

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Acute Mastoiditis
• May extend in the sheath of
sternocleidomastoid (Bezold’s abscess).
Postaural abscess
Bezold’s abscess
Spread of Mastoid abscess - 4

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Acute Mastoiditis
• Extends toward petrous apex  petrous
apex abscess  may involve the V and VI
CN’s to produce Gradinego’s syndrome.
Spread of Mastoid abscess - 5

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Acute Mastoiditis
Clinical features
Sign & Symptoms;
• Fever, deafness, otalgia;
(Severe pain behind the ear and tenderness
over the mastoid region).
• If subperiosteal abscess is present, pinna
protrudes forward and there is fluctuant
swelling in the postaural area.
• Discharging fistula may be seen
• Other local signs depend on stage and severity of
infection.

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Acute Mastoiditis
Management
• Antibiotics , are used in early stage in same
way as used for Acute otitis media.
• Incision & Drainage is done immediately to
evacuate the pus if abscess is present.
• Cortical mastoidectomy to evacuate the pus
from the mastoid antrum is indicated if there
is no improvement seen with the appropriate
antibiotic treatment.

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Otitis Externa
• Purulent material discharging from the Middle
ear may accumulate in the EA Canal.
• This leads to development of otitis externa and
may predispose development of fungal infection.

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Thrombosis of I.J.V.
• This usually occurs as downward extension
of the thrombosis of the sigmoid sinus.

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Petrositis

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Petrositis
• Not seen very frequently these days
• It occurs due to direct extension of the
infection from the middle ear to the
pneumatized petrous bone.
• The infection may remain confined to the
petrous bone or extends intracranially.
• It may spread downwards to form abscess
in the pharynx.
Introduction

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Petrositis
• Initial
– clinical features are those of Acute otitis media
• Later on
– Severe unilateral headache in the temporal, supra-
orbital or retro-orbital region, this is due to the
irritation of the trigeminal nerve ganglion
– Paralysis of VI cranial nerve; diplopia.
• Gradinego's syndrome : (otorrhea, pain in
the distribution of trigeminal nerve, diplopia)
Clinical Features

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Petrositis

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Petrositis

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VI nerve palsy
Petrositis
Gradinego's
syndrome
Otorrhea pain

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– Medical treatment is same as for acute
otitis media
– Surgical drainage is indicated in some
cases
Petrositis
Treatment

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Chronic Adhesive Otitis Media
• Adhesions may form within the middle ear
as a result of chronic or recurrent infections.
• Adhesive otitis media is characterized by
atrophic changes and a partial or complete
retraction of the tympanic membrane toward
the medial wall of the tympanic cavity.
• There is atrophy (or thickening) of the TM
with significant conductive deafness.

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• The TM is bound to the medial wall of the
middle ear by fibrous adhesions,
• There is no possibility of reversing the
retraction by re-aerating the middle ear.
• Treatment
– Tympanotomy  surgical divisions of adhesion
 placement of silastic sheet within the middle
ear.
Chronic Adhesive Otitis Media

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Old Adhesive Otitis Media
with Myringostapedopexy

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Thin atrophic tympanic membrane has retracted
and is adherent to the promontory. Several
patches of tympanosclerosis are visible anteriorly.

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Facial Nerve paralysis
Can be caused by ;
1. A.S.O.M.
2. C.S.O.M. with/ without Cholesteatoma.
3. Surgery on the middle ear and mastoid

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Facial Nerve paralysis
1. In ASOM it is secondary to the pressure of
the pus on the nerve
– Generally seen with dehiscent facial nerve.
– Usually recovers as the acute infection settles.
2. In CSOM the nerve is affected due to
erosion of its bony canal by cholesteatoma,
– Initially it is only compressed but later on it may
be destroyed, hence the recovery is poor.
– Surgical removal of cholesteatoma is necessary.

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Facial Nerve paralysis
3. Facial nerve can also be paralyzed due to
damage caused by surgery done on the
middle ear and mastoid.
– Severity varies from mild weakness to complete
paralysis.
– If there is complete paralysis found immediately
after surgery  immediate exploration is
recommended.

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Labyrinthitis
• Suppurative inflammation of the
membranous labyrinth of the inner ear
• Infections secondary to AOM or CSOM
spreads through;
– the oval /round window
– Bony erosion due to cholesteatoma
(fistula formation)
– After surgery on cholesteatoma

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Labyrinthitis
Clinical Features
• Vertigo
• Nausea & Vomiting
• Deafness
• Nystagmus
• Total SNHL in advanced stage

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Labyrinthitis
Treatment
Medical treatment
• Antibiotic therapy
• Antivertiginous drugs
Surgical treatment
• If fistula formation is there

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1. Extradural abscess
2. Lateral sinus thrombosis
3. Meningitis
4. Subdural abscess
5. Brain abscess
6. Otic hydrocephalus
Intracranial
Complications

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Extradural abscess
• Pus collection between bone and dura
• May remain silent, symptom-less
• Discovered during surgery
• Deep seated otalgia, Low grade fever,
pulsatile discharge.
• No localizing SS
• Remove necrosed bone, drain abscess,
consult neurosurgeon if very large

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Lateral sinus thrombosis
• Uncommon, usually follows CSOM.
• Development of infected clot in lumen of sinus  may
release organisms in systemic circulation 
bacteremia, septicemia & septic embolization.
• CF; vague, usually masked by A/B; fluctuating
pyrexia, rigors and headaches over week with ear
discharge. Tenderness along IJV, papilloedema, visual
loss …
• Contrast CT is diagnostic, MRI
• Antibiotics, Mastoidectomy, explore the sinus

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Meningitis
• Can occur with AOM,
• BUT more common with CSOM
• Fever, headache, neck stiffness, kerning’s
sign
• Varied level of consciousness: irritability/
confusion/ drowsiness / drowsy/unconscious
• Signs of raised ICP, focal neurological palsies
• LP, CSF examination: DR, C/S
• Antibiotics, treat primary cause

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Subdural abscess
• Extremely rare, serious,
poor prognosis
• Pus between dura & arachnoid
• Extremely ill, severe headache, fever, Signs
of raised ICP: Bradycardia, Papilloedema
• Focal neurological signs: hemiplegia…
• Drowsiness, coma, epileptic fits
• Ref to neurosurgeon: Immediate drainage

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Brain abscess
• Collection of pus within the brain
tissues
• Temporal lobe & cerebellum favoured
sites
• 50% of adult brain abcesses are
otogenic. 25% in children

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Temporal lobe abscess
• Commoner
• Dysphasia/ Aphasia: if
involves speech area in dominant hemisphere
• Homonymous Hemianopia: if involves fibers
of optic radiations
• Contralateral paralysis of limb: if involves
internal capsule
• Epileptic fits, coma, high grade fever

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Cerebellar abscess
• Raised ICP; occipital headache,
vomiting, papilloedema, high
grade fever, bradycardia
• Drowsiness, confusion, lethargy, coma
• Cerebellar signs: Ataxia, nystagmus, past
pointing, dysdiadokokinesis, + Romberg’s
sign
• CT, MRI, CSF analysis
• Neurosurgical intervention

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Sigmoid Sinus thrombosis
• Rare nowadays
• OM mastoiditis infl. of walls
of sinus thrombus within sinus
rapid enlargement, blocked lumen  may
involve IJV/ cavernous sinus
• Symptomless in early cases: esp. wi AB therapy
• Fever with rigors, headaches, vomiting
• Raised ICP, septicemia
• Tenderness along jugular vein
• Anticoagulants, evacuation of thrombus

58. Thank you
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