Complication of

Suppurative Otitis Media

 History
• Hippocrates : 460 BC
• Brain abscess : first to be recognized and
operated
• 1768 : Morand operated brain abscess
• 1856: Lebert describe pathology of brain abscess
• 1881 : MacEwean ; series of brain abscess optd
• 1935 :introduction of sulphonamides
• 1942: Penicillin introduced : incidence decreased
 Introduction
• When infection spreads outside the confines
of bony wall of middle ear and mastoid spaces
• Can involve intracranial structure and
structures with in the temporal bone
• Any CSOM ear can cause the complications
however CSOM with cholesteatoma more
• more found in males
Sites for spread
Classification
 Route of spread
• Pathological bony defects
• Thrombophlebitis , Periphelebitis
• Normal anatomical pathways : OW,RW
• Non anatomical pathways : trauma,
accidental, neoplastic erosion,Iatrogenic
• In brain tissue: spreads via periarteriolar
spaces of Virchow-Robin
Route of spread
 Factors
• Immunity level of individual
• Virulent strain of organism
• Availability of treatment
 General Principles
• Symptoms
Mortality rate : about 19 %
Early
– Aural discharge with fever & headache
– Otalgia and vertigo
Late
– Decreasing levels of consciousness and
convulsions
 Microbiology
• Complicated ASOM
H. Influenzea , Str. Pneumoniae
Also streptococcus,Staphylococcus

Complicated CSOM :
Gram negative & anerobes:
Pseudomonas aeruginosa, Proteus sp
Str milleri , Bacteriodes
 Investigations
• Routine inv.
• Culture of aural discharge and blood
• X ray mastoid:
• HRCT: axial and coronal sections
Plain and contrast
• MRI
• DTPA
• Lumbar puncture
 Treatment
• Early diagnosis
• Help from Neurosurgeon
• Treatment of underlying ear disease: should
be secondary to neurosurgical intervention
• Intravenous combination high dose antibiotics
therapy
 Epidural (Extradural Abscess)
• One of the most common
• Direct extension
• Middle fossa EA:
Erosion of tegmen tympani
Petrous pyramid -> Trautmann triangle -
>
Trigeminal Ganglion & VI nerve ->
Gradenigo Synd
(otrrhoea+facial pain+diplopia)
Abscess is well encapsulated
• Posterior fossa abscess:
Lateral sinus -> lateral sinus thrombophelbitis

Symptoms : non specific , discharge ( creamy &

pulsatile)
Dull headache
often incidental finding
TT : Ab & Surgical Drainage
Mastoidectomy approach
 Subdural Abscess
• Infection through dura
• Abscess between dura and arachnoid
• Dura -> infflm reaction ->granulation tissue -> fibrous
tissue -> Necrosis of dura -> abscess in subdural
compartment
CF : rapidity of neurological deterioration
Hemiplegia or Jacksonian convulsions
Inv: CSF,CT scan , Fundoscopy
TT: multiple burr holes or craniotomy & abscess excision
Post operative Anti convulsants
 Lateral Sinus thrombosis
• Formation of thrombus in lumen of the sinus -
> release of organism -> septicemia
• Cranial extension : Sagittal Sinus Thrombosis
Petrosal sinus ->
Cavernous sinus
• Caudal extension : Internal Jugular vein &

subclavian vein
Intracranial Venous Sinuses
CF :
• wasting illness with fluctuating pyrexia with chills
and rigor developing over several weeks
(Picket fence fever),Headache,Progressive anemia
• Tenderness along IJV (Sternocleidomastoid)
• Sig ST : papilledema & visual loss
• CST : Proptosis or Chemosis
• Gresinger sign : pitting edema around the occiput due
to thrombosis of large mastoid emissary vein
• Tobey-Ayer Test: positive( Absent)
• Crowe-Beck test :
Tobey-Ayer Test
• Inv :
– Hb, peripheral smear, fundoscopy
– X ray mastoid:
– CT Scan: Delta Sign : in axial cuts: enhancement of
sinus walls but not the content ; Filling defect
– MRI with contrast- thrombus
• TT :
• Ab & Surgery :thrombus removal
• Anticoagulant: if CS is involved
• IJV ligation : if septicemia fail to respond to AB
 Meningitis
• Most common complication :
• Spread : direct -> tegmen plate
sinus plate -> labyrinth
CF : headache ,neck stiffness & photophobia
alternating restlessness & drowsiness
High pyrexia and vomiting
Kernig sign: + ve
Inv : CT normal, MRI : abnormality in basal cistern
Lumbar puncture: CSF : decrease: glucose
increase : protein
TT: Repeated LP, Steroids
Surgery
 Brain Abscess
• Adults :Complicated CSOM principal cause
• Children : Cong Heart ds,
• Mortality : 10-20%

• Temporal lobe Abscess ( MC): Tegmen tympani

• Cerebellar Abscess(lateral lobe) ; LST

• developed after 1-3 weeks

• Routes
Pachymeningitis -> Thrombophlebitis-> cerebral cortex
Periarteriolar Virchow Robin space
• Pathology
• Stage of Encephalitis: headache, fever, vomiting
• Stage of localization(capsule) : asymptomatic period
• Stage of enlargement : mass effect ->CSF-> ICT
• Stage of rupture :
TLA : rupture in to lateral ventricle, cerebral
surface
CA : rupture in to IV ventricle
• CF
Raised ICP:
Headache, malaise, nausea, projectile vomiting,
Fever: low grade, hypothermia,
Bradycardia, Papilloedema,
Apathy,drowsiness,delirium,convulsions
TLA;
dysphagia,Homonymous upper quadrantic hemianopia,
Jaksonian convulsions, hallucination of smell and taste,
Nominal Aphasia in Lt temporal abscess
• CA :
Headache : suboccipital radiate down to neck
Weakness and loss of tone on affected side
Vertigo , nystagmus , ataxia
Past pointing test impaired
Inv : CT : abscess with enhancing capsule with
surrounding oedema
MRI
TT : raised ICT : steroids and mannitol
multiple burr holes & abscess excision
Stereotactic aspiration: TOC
Anticonvulsant therapy
 Otitic Hydrocephalus
• Rare :
• found mostly in children
• Benign Intracranial HTN
• LST -> Sig ST ->impairment in CSF resorption ->

raised ICT
• Gradual onset varying to weeks or yrs
• CF of raised ICT
• CT : normal ventricles size
• TT : Steroids ,diuretics ,peritoneal shunting
THANX
Complication of Suppurative
Otitis Media
(Intratemporal)

DR HARVINDER KUMAR
PROF & HEAD
ENT,PIMS
 Intratemporal Complications
• Acute Coalescent mastoiditis ,
• Masked mastoiditis
• Subperiosteal Abscess (Postauricular abscess
Bezold’ s abscess & others)
• Petrositis (Petrous apicitis )
• Acute suppurative labyrinthitis & Labyrinthine
fistula
• Encephalocele and cerebrospinal fluid leakage
• Facial nerve paralysis
 Acute Coalescent mastoiditis
• This is an acute progressive clinical infection with
corresponding changes in the bone and mucoperiosteum of
the mastoid air cell system causing coalescent of mastoid
air cells due to the destruction of bony partition

• This is a disease of the young, mostly males & most

patients are 6 years old or younger.

• MC cause is complicating ASOM

• Bacterial virulence and decreased host resistance are

important factors
• Usually takes 2 to 4 weeks to develop after the initial
infection
 Microbiology
• Similar to those found in most cases of ASOM
H. Influenzea , Str. Pneumoniae
Also Streptococcus,Staphylococcus,

Gram negative & anerobes:

Pseudomonas aeruginosa, Proteus sp
E.Coli
 Acute Coalescent mastoiditis
Mastoid development plays a role.
• The condition rarely develops in children who
have had chronic ear disease or in those with
poorly pneumatized mastoids containing few air
cells.
• It tends to occur in patients with well-developed
air cell systems that contain numerous small
pneumatic spaces and in those who have had
little or no previous otologic disease.
 Pathology
• As the infection grows , inflammatory empyema
pressure within the mastoid cavity increases
,which extend beyond the confines of the
mastoid.
• Modes of spread:to other structures
• Phlebitis and periphlebitis are common :
Spread the infection to the adjacent
meninges, sigmoid sinus, cerebellum, and temporal
lobe.
• By Bone erosion :
The infection extends directly to the
meninges, sigmoid sinus, labyrinth, or facial nerve
Pathology
Progression of Acute Mastoiditis
 Clinical features
• Profuse Purulent otorrhea, fever, toxicity, and ear pain—
as those seen in patients with uncomplicated AOM.
• Mastoid reservoir sign: Persistent discharge not responding to
the treatment.
• The chronology of the infection in which purulent discharge or
significant otalgia persists for 2 or more weeks, recurs after 10
to 14 days, or worsens after that time interval.
• Children look sicker and have more toxic looks.
• Physical findings that are most helpful :
mastoid tenderness,
mastoid erythema, and
Sagging of the posterior superior
deep meatal wall.
 Treatment
Inv : TFT, Xray B/L Mastoid, CT
Medical and surgical.
Complete Mastoidectomy with ventilating tube
placement in conjunction with
• Appropriate IV Ab for a minimum of 3 to 6 weeks: To
eradicate the disease process in the majority of
infected patients who have no additional
complications.
• The patient should continue receiving Ab therapy until
a CT scan produces evidence that the mastoid air cell
system is no longer opacified and the middle ear is
normally aerated.
 Masked mastoiditis
Chronic otitis media with bone erosion and
granulation tissue formation without otorrhea.
TM : normal or near-normal or perforation fail
to heal
It usually occurs in patients who have received
numerous courses of Abs.
The epitympanum and aditus become blocked
so that the middle ear responds to the Abs, but
the mastoid does not.
 CF
Patient has persistent aural and postauricular
Pain , & definite tenderness over the mastoid
cortex,
Generalised malaise with low grade fever
Plain mastoidradiographs:
CT scan:
• evidence of very localized areas of
opacification in an otherwise normal mastoid
• Also show underlying ds & any complication , if
any
 Differential Diagnosis
• Furunculosis with
cellulitis
• Sebaceous cyst
• Post auricular
lymphadenitis
• There are two keys to the successful
management of masked mastoiditis:
(1) Disease is not always reflected by the
appearance of the tympanic membrane,
(2) chronic mastoiditis is a surgical condition,
regardless of the appearance of the tympanic
membrane.
• Initial IV Antibiotics : if no improvement or
worsening of symptoms , then
• Cortical Mastoidectomy :
– Drainage of pus : emergency
– Exenteration of mastoid air cells
– Opening of the mastoid antrum and producing a
widely pneumatized tract from middle ear to mastoid
• EUM : TM inspected: if intact: myringotomy with
ventilation tube insertion
 Post auricular abscess
• Post auricular abscess is the most common
complication of mastoiditis.
• It is most often seen accompanying
coalescent mastoiditis in young children.
• The infection extends from the mastoid to the
subperiosteal space. Usually, this occurs by
direct extension subsequent to bone
destruction or by phlebitis and periphlebitis of
mastoid veins
• Soft tissue infection leads to tissue necrosis
and abscess formation -> skin ->
Post auricular fistula :
• The surrounding soft tissue develop abscess
which will exhibit thickening, inflammation,
erythema , tenderness, and fluctuance
• The auricle is pushed downward and laterally.
• TT : excision and drainage in conjunction with
Mastoidectomy
 Other abscesses
• Von Bezold’s abscess :
The cervical infection develops by an abscess
in the upper neck anterior & deep to the
sternocleidomastoid muscle.
Can develop with perforation and necrosis of
mastoid tip or without any erosion or penetration
of the inner and outer cortex of the mastoid
through phlebitis and periphlebitis transmits the
infection
Bezold’s abscess occurs more commonly in older
children
• in young patients with deep, tender, upper
cervical masses
• CT Scan : If diagnosis is not clear
• TT: complete surgical excision of the mastoid
pathology, drainage of the abscess, and
removal of any associated granulation tissue
• Citelli’s abscess : when pus extend along the
digastric muscle in to the submandibular
triangle
• Zygomatic abscess: anteriorly to zygomatic
process
• Luc’s abscess : external auditory canal
• Pharyngeal abscess :
 Petrositis
PETROUS APICITIS
• Petrous apicitis is essentially mastoiditis that
occurs in the petrous apex.
• A petrous apex can be undeveloped (sclerotic), or
can exhibit some degree of pneumatization.
• Pneumatization of the petrous apex : 30%
• Pneumatised chains: 2 chains
– 1) Posterosuperior chain:attic & antrum,around
semicircular canals -> apex
– 2) Anteroinferior chain : hypotympanum,eustachian
tube around cochlea -> apex
• Petrositis develops by direct extension of a
mastoid infection
• It is rare :
– infection in sclerotic or marrow-containing
petrous apices is uncommon because
pneumatization is less.
– the mastoid may respond to medical or surgical
treatment without resolution of the apical
infection.
Pathology:
• As seen in coalescent mastoiditis with
dissolution of thin cellular septi and
coalescence, or form granulation tissue and
erode bone like in ch mastoiditis.
• Rarely cholesteatoma extend to the apex.
• CF : 3 D’s
– Discharge , Deafness, diplopia,
• The most common symptoms from infection in the
petrous apex are deep seated retroorbital pain from
irritation of the trigeminal ganglion in Meckel’s cave,
• Paralysis of the sixth cranial nerve as it passes through
Dorello’s canal
• Dysfunction of the facial , acoustic, or vestibular nerves
during their course through the temporal bone.
• In 1904, Gradenigo described the syndrome:
– triad of retro-orbital pain, sixth nerve paralysis, and
otorrhea,
Others : fever ,malaise & vomiting
Imaging studies :
• CT scan : Show the bony details of the septae
of the air cells and the size
and contour of the
apex as a whole.
• MRI : Differentiate marrow from mucus or
CSF.
• Both CT and MRI is essential for the diagnosis
TT ;
• IV antibiotics
• Complete cortical mastoidectomy &
skeletonization of SCC & exploration of tract of
infection up to the apex.
• Approaches : The posterosuperior route
– Frenckner : under arch of Sup SCC
– Raminder-Lempert : between ICA & Cochlea
– Thornval : Under middle fossa dura
 Labyrinthitis
• Inflammation of labyrinth
• Bony erosion of Otic capsule : CSOM
• Routes: mc through round window
membrane , OW nice –
surgery
• MC site : Lateral SCC
• Types:
– Serous Ly
– Otogenic suppurative Ly
– Meningitic suppurative Ly
• Spread of pyogenic organisms & their exotoxins in the
Ly causes severe insult to the vestibular & cochlear
neuro-epithelium that almost invariably results in
permanent vestibular & cochlear failure
I 
prompt treatment
-----------------------------------------------
Reversible
Non-reversible
Serous Ly
Suppurative Ly
• Diagnosis is retrospective
 CF
Symptoms:
• Recurrent attacks of dizziness & nausea aggravated on
head movements later to frank vertigo
• Ds is confined to ear :Temp remains normal
• Hearing is normal in earlier stages but may worsen as
ds progress & cause Mild CD to profound SNHL from
temporary to total & permanent HL
• In Chronic form : the symptoms are insidious in onset
due to compensatory action of opposite labyrinth
• Position of patient in acute stage: curled up in bed lying
to the side of normal ear & affected ear above
Signs :
Spontaneous horizontal nystagmus to the diseased ear : during the
attacks
Fistula sign: + ve to –ve
Inv:
CT scan of temporal bone:
Audiogram , CSF ex
T/T : initially medical:
Bed rest, IV Ab, vestibular sedatives like
prochlorparazine
Later surgical : if pt not responding to tt & essentially after
vertigo has subsided
 LABYRINTHINE FISTULA
• Erosion of the bony labyrinth. The loss of this bone
allows the underlying endosteum, perilymph, and
structures of the endolymphatic compartment to move
when the pressure in the EAC is changed.
• Motion of the fluids in the endolymphatic compartment
brings on the symptoms of labyrinthine fistulae.
• Almost all labyrinthine fistulae affect the arch of lateral
semicircular canal; the superior and posterior
semicircular canals, vestibule, and cochlea are rarely
involved.
• Cholesteatoma is the cause in nearly all cases
 Fistula Test
Fistula test,
The examiner occludes the external auditory canal with
the pneumatic otoscope and alternately increases and
decreases the pressure slightly so that pressure changes
are transmitted from the canal to the middle ear through
either an intact or a perforated tympanic membrane.
During the test, the patient is told to look directly ahead
at a specific object, and the physician ( better if 1
observer is present) observes the patient’s eyes for any
horizontal deviation.
In a normal ear, changes in external canal pressure cause
no motion of the eyes and no vertigo
 Interpretation
Positive fistula sign,
Positive pressure :Conjugate deviation of the eyes
away from the side of the compression --> towards
unaffected side
Pressure is maintained: jerky movement to & fro
If pressure is released : eyes return to midline
The nystagmus is accompanied with vertigo
The patient may become slightly dizzy & nauseate
Only 55 to 70% of patients with lateral canal
erosions have a positive fistula test
• Lateral canal fistula : anterior to ampulla:
towards affected side
Superior canal fistula:
rotatory deviation from affected side
Posterior canal fistula:
vertical deviation
Vestibule :
rotatory horizontal deviation towards
the affected side
• False –ve fistula sign:
 if seal of speculum inadequate
 fistula is covered by epithelial debris
or
granulation tissue
 Dead labyrinth
• False +ve fistula sign:
Hennebert sign:
present of intact TM
early congenital syphilis due to lax & mobile
annular ligament
Hyper mobile stapes

Tullio’s phenomenon : Patient feel suddenly off

balance when they hear a sudden loud sound,
• Labyrinthine fistulae cause mostly vestibular symptoms.
• MC is short lived episodic vertigo
Patients describe short periods of imbalance,
disequilibrium, or vertigo but have normal
equilibrium most of the time.

• Inv : CT Scan : 300 tilted axial scan

Definitive
diagnosis: on surgery
TT: surgical exploration
• Canal wall down
• Canal wall up
• removes all of the cholesteatoma except for a
small area around the fistula site
• A small piece of tissue or a thin cap of bone or
temporalis fascia graft is placed over the site
after the cholesteatoma is successfully
removed.
• Encephalocele (brain hernia, brain fungus,
meningoencephalocele) &
CSF leakage may be associated with other
cranial or intracranial complications in acute or
chronic otitis media.
• Three different clinical patterns can occur.
 Spontaneous CSF leakage
• Spontaneous CSF leakage
• from defects in the tegmen tympani
• 70 to 80% of the patients are over 45 years of age.
• The defects range in diameter from 2 mm to 2 cm and
are sometimes multiple.
• Usually an encephalocele protrudes through the
defect.
• Patients may present with signs and symptoms of
meningitis
• Myringotomy and placement of a ventilating tube
release a profuse watery otorrhea that tests positive
for CSF
Encephalocele and CSF leakage secondary to
chronic otitis media
• Occur when a cholesteatoma and granulation
tissue erode through the bony plates that
separate the mastoid from the temporal lobe and
then erode through the dura.
• The mastoid and epitympanic tegmen are
involved more frequently
• It usually takes many months to years for
cholesteatoma to cause this degree of bone
erosion,and dural erosion.
Traumatic encephalocele and CSF leakage
most common
• May occur secondary to temporal bone fracture,
• The great majority are the consequence of an
operation in which portions of the tegmen or
cerebellar plates were removed and the dura was
exposed or traumatized.
• In these cases, both the disease process and the
surgery contribute to the bony and dural traum &
development of an encephalocele, CSF leakage,
and intracranial complications
Management:
• Prompt surgical repair
• Factors :Size of the bony defect and
the volume of herniated brain.
• Small defects :
managed through the mastoid,
• Multiple and large defects :
best repaired by combination of
transmastoid and middle cranial fossa approaches. (Combined
transmastoid intradural middle cranial fossa approach)
• To reduce the risk of infection, the defects are usually
repaired with autogenous graft materials.
Thanks